Diabet, Nutriţie, Risc Cardiometabolic

Transcription

N um ă ru l 2 , Se p t e m B r i e 2 0 1 0
Diabet, Nutriţie,
Risc Cardiometabolic
2
Organ al Federaţiei Române de Diabet,
Nutriţie şi Boli Metabolice şi al
Asociaţiei Germano-Române pentru
Cercetarea Complicaţiilor Diabetului Zaharat.
Diabetes, Metabolism, and the Heart
(Diabetes, Stoffwechsel und Herz)
R e v i s tă d e c a r d i o d i a b e t o l o g i e ş i d o m e n i i a s o c i at e
Cercetare · Îngrijire medicală · Management
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The 25 Symposium of the Federation of
International Danube-Symposia on Diabetes Mellitus (FID)
and the 5th Congress of the Central European
Diabetes Association 2010
th
Pr eface s / Cu v i n te I na i n te
Th e FID M e eti ng 2 010
N. Hâncu, A. Ştirban:
Dear FID Participants, dear Colleagues
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N. Hâncu, I. A. Vereşiu:
Dear Colleagues and Friends
The 25th Symposium of the FID and the 5th Congress
of the Central European D
iabetes Association 2010,
Cluj-Napoca, Romania:
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Scientific Program
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Abstracts of the Oral Presentations
65
Abstracts of the Poster Presentations
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M. Roden, N. Schloot:
Dear Members and Friends of the Central European
Diabetes Association-FID
www.diabetzaharat.info
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R e dac ţ i a ş i e d i t u ra
Redacţia şi editura:
Verlag Kirchheim + Co GmbH,
Kaiserstr. 41, D- 55116 Mainz/Germania
Tel. +49 - 61 31/ 9 60 70-0,
Fax +49 - 61 31/ 9 60 70 70,
E-Mail: [email protected],
Internet: www.kirchheim-verlag.de
Co-Redactori-şef:
Nicolae Hâncu, Cluj-Napoca, Romania
Alin Ştirban, Bielefeld, Germania
Diabet, Nutriţie,
Risc Cardiometabolic
Diabetes, Metabolism, and the Heart
(Diabetes, Stoffwechsel und Herz)
Secretare generale ale redacţiei:
Cornelia Bala - Cluj-Napoca
Cristina Niţă - Cluj-Napoca
Redactori:
Anca Buzoianu - Cluj-Napoca, Gabriela Creţeanu Suceava, Dan Gaiţă - Timişoara, Carmen Georgescu
- Cluj-Napoca, Dan Gheorghe - Bucureşti, Mariana
Graur - Iaşi, Radu Lichiardopol - Bucureşti, Maria
Moţa - Craiova, Monica Negrean - Bad Oeynhausen,
Amorin Remus Popa - Oradea, Gabriela Roman Cluj-Napoca, Carmen Săndică - Bad Oeynhausen,
Eugen Săndică - Bad Oeynhausen, Lorant Szentagotay
- Cluj-Napoca, Ioan Andrei Vereşiu - Cluj-Napoca,
Dragoş Vinereanu - Bucureşti.
Colectivul ştiinţific:
Oliver Schnell - München (G), Diethelm Tschöpe Bad Oeynhausen (G), Andreas Pfützner - Mainz (G),
Martin Lederle - Stadtlohn (G), Rodica Pop - Buşui,
Michigan (USA), Ronald Tamler - New York (USA).
Diabet, Nutriţie, Risc Cardiometabolic este varianta
în limba română a jurnalului „Diabetes, Stoffwechsel
und Herz“, Germania, indexat în Science Citation
Index Expanded, Journal Citation Reports/Science
Edition, EMBASE/Excerpta Medica.
www.ds-herz.de
2
Organ al Federaţiei Române de Diabet,
Nutriţie şi Boli Metabolice şi al
Asociaţiei Germano-Române pentru
Cercetarea Complicaţiilor Diabetului Zaharat.
R E V ISTĂ D E C A R D IO D I A B ETO L O G IE Ş I D O M ENII A SO C I ATE
Cercetare · Îngrijire medicală · Management
Pr eface s / Cu v i n te I na i n te
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Organizaţii asociate acestui număr:
EASD Diabetes & Cardiovascular Disease Study
Group
Director al editurii:
Manuel Ickrath (G)
Contents / Conţinut
N. Hâncu, A. Ştirban
Dear FID Participants, dear Colleagues
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N. Hâncu, I. A. Vereşiu
Dear Colleagues and Friends
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M. Roden, N. Schloot
Dear Members and Friends of the Central European Diabetes Association-FID
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Th e FID M e eti ng 2 010
Apariţie:
frecvenţa apariţiilor va fi iniţial de 4 jurnale pe an.
The 25th Symposium of the FID and the 5th Congress of the Central European
Diabetes Association 2010, Cluj-Napoca, Romania:
Printare:
Studio Impress Design srl, 400221 Cluj-Napoca,
România
Scientific Program (all sessions in English or German with translation)
61
Abstracts of the Oral Presentations
65
Abstracts of the Poster Presentations
70
Drepturie conform legii rămân în posesia Editurii
Kirchheim (numită Editură). Anumite contribuţii
marcate corespunzător nu reproduc în totalitate
părerea editurii. Jurnalul, precum şi toate contribuţiile
şi imaginile conţinute, sunt protejate prin drept de
autor. Reproducerea ilegală în totalitate sau parţial a
conţinutului jurnalului fără acordul Editurii poate fi
urmărită în justiţie. Conţinutul reclamelor reproduse
în acest jurnal nu sunt responsabilitatea Editurii ci a
autorilor ei. Reclamele reflectă în totalitate punctul de
vedere al acestora.
© Kirchheim-Verlag, Mainz/Germania
Diabet, Nutriţie, Risc Cardiometabolic, Numărul 2/2010 www.diabetzaharat.info
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P r e fa c e s / C u v i n t e î na i n t e
Dear FID Participants, dear Colleagues,
Prof. Dr.
Nicolae Hâncu
Co-Editor-in-Chief
Cluj-Napoca, Romania
Let us begin by warmly welcoming to
our city, Cluj-Napoca, all the participants of the 25th Symposium of the
FID and the 5th Congress of the Central
European Diabetes Association. It is a
great pleasure for us to have you here
and a challange to prepare this issue of
our journal dedicated to this scientific
event. We are proud to have the chance
to publish exciting results generated by
researchers from all over Europe and
are convinced that many of our young
colleagues who entrusted us their abstracts will represent the future leading
scientists and opinion leaders not only
in their countries, but also internationally.
great history. You can read more about
the FID on the official website:
www.fid.at. There you can also find
information about how to become a
member of the international community of the FID.
We wish you a pleasant lecture and a
great time in Cluj-Napoca!
Sincerely yours,
Prof. Dr. Nicolae Hâncu
Co-Editor-in-Chief
Cluj-Napoca, Romania
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Dr. med.
Alin Ştirban
Co-Editor-in-Chief
Bielefeld, Germany
Beyond unifying cultures and research
from entire Europe, one of the qualities of the FID is to actively support
young researchers to present the results
of their work. This ‘young spirit’ goes
through the many abstracts we have
received and witnesses for the richness
of ideas that characterizes this generation of researchers. As you will be
able to find out, the topics are various,
reaching from basic science to clinical
science and epidemiology. Therefore,
we are confident that everyone will find
topics of interest.
Dr. med. Alin Ştirban
Co-Editor-in-Chief
Bielefeld, Germany
But there is no successful young generation without a generation of mentors
behind. Reading the congress program,
you will find renowned names of mentors that have not only formed generations of scientists, but also decisively
impacted on the European and mondial diabetology of the last decades. We
are privileged to have them in Cluj-
Napoca!
To those just reading this issue of our
journal, we hope to provide not only
interesting scientific information, but
also an insight into the spirit of the Federation of International Danube Symposia (FID), an organization that has a
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C u v i n t e î na i n t e / P r e fa c e s
Dear Colleagues and Friends,
Prof. Dr.
Nicolae Hâncu
First of all, we wish to thank all of you
who accepted, by registering and/or
sending the abstracts of their work,
to attend the this year’s meeting of the
FID in Cluj-Napoca. We are aware that
the postponing of the traditional date
of FID meetings (due to the late June
ADA meeting this year) has generated
some confusion and we apologize once
again, but the high number of abstracts
received demonstrates that this inconvenient was minor. The 54 abstracts
were carefully evaluated by a committee
of German and Romanian colleagues.
As you can see in the congress program
(in this journal and on the FID 2010
website: www.fid2010.org), there will
be two sessions dedicated to oral presentations, since eight of the received
abstracts were chosen for these ses
sions. The rest will be presented in the
poster sessions. We hope that the topics
of these presentations, together with
the topics of the sessions having invited
speakers, are covering many actual
basic and clinical aspects of diabetes
and its complications and will stimulate
discussions during the meeting. You
will probably agree that we are living
challenging times being contemporary
with a continuous increase of diabetes
prevalence; we are using more and
more new antihyperglicaemic drugs
and the issues of cost/effectiveness and
risk/benefit confronts all practitioners;
and, last but not least, basic researchers
are doing a great job in their attempt
to answer the numerous questions
on pathomechanisms of diabetes and
treatment options.
As you know, Central and Eastern
European research and clinical
practice in the field of diabetes and
other metabolic diseases have many
similarities in the various countries
of the area, but lately, different characteristics also emerged. One of the
missions of the FID is to explore them
and allow its members to share their
positive experience with each other.
This important topic will represent
the essence of a round table discussion,
where we will have the chance to listen
to known opinion leaders, past-presidents and founders of the FID, people
who witnessed how our organization
developed and metamorphosed, but
also to the thoughts of young diabetes
researchers.
We can assure you that we will do our
best to organize for you that kind of
meeting that unifies the ‘Mitteleuropa’
professional and living spirit, and we
hope that at the end you will be able
to say that our efforts were – at least in
part – successful.
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Assoc. Prof.
Ioan Andrei Vereşiu
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www.diabetzaharat.info
Prof. Dr. Nicolae Hâncu
Assoc. Prof. Ioan Andrei Vereşiu
Co-Presidents of the Local
Organizing Committee
Diabet, Nutriţie, Risc Cardiometabolic, Numărul 2/2010
P r e fa c e s / C u v i n t e î na i n t e
Dear Members and Friends
of the Central European Diabetes Association – FID,
It took a long time until the country
where the Danube flows into the Black
Sea, hosts for the first time the International Danube Symposia on Diabetes mellitus as well as the Annual Meeting of the Central European Diabetes
Association – FID. I am really looking
forward to further deepen our friendly
relationship related to diabetes research
with Romania on this occasion taken
place in Cluj-Napoca from September
9th to 11th, 2010.
our association and in Romania, but
also between the younger colleagues
addressing questions for future diabetes
research and practice!
In the early 20th century, research on
insulin was tightly linked to Romania. But also today, Romania is getting
more and more involved into European
diabetes research. This is further underlined by the fact that our meeting
will be held in connection with the 5th
Congress of the Romanian Federation
for Diabetes, Nutrition and Metabolic
Diseases.
PD Dr. Nanette Schloot
General Secretary of the Central
European Diabetes Association – FID
Duesseldorf
With best Central European regards.
Univ.-Prof. Dr. Michael Roden
President of the Central European
Diabetes Association – FID
Duesseldorf
Univ.-Prof. Dr.
Michael Roden
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Our FID meeting will address – on top
of the classical diabetological topics –
the opportunities for mutual cooperation within FID, as well as for training
and development of young colleagues.
To this end, a ‘round table’ session including founders and previous presidents of FID as well as young researchers was organized to discuss the future opportunities for and within FID.
PD Dr.
Nanette Schloot
It is therefore my great pleasure to look
forward to the meeting in Cluj-Napoca, which will allow for intensive interaction and exchange among those
who have been active in diabetes in
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Scientific Program / Program ştiinţific
The 25th Symposium of the FID and the
5th Congress of the Central European Diabetes
Association 2010
9 – 11 September 2010
Cluj-Napoca (Klausenburg), Romania, Grand Hotel Napoca
Scientific Program (all sessions will be held in English or in German with translation)
D a y 1 : T h u r sd a y , S e p t 9 , 2 0 1 0
13.00 – 14.00
12.00 – 14.30 14.30 – 15.00
Opening ceremony
15.00 – 16.30: Session I
Hot topics Doctor honoris causa ceremony for Prof. Helmut Schatz
Location: Multimedia Hall, “Iuliu Haţieganu” University of Medicine and Pharmacy Cluj-N.
(For invited persons)
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Lunch
FID ’From Tradition to Transition‘
• Official persons (Rector of ’Iuliu Haţieganu‘ Univ of Med and Pharm Cluj-Napoca)
• Congress Presidents: N. Hâncu, I. A. Vereşiu
• FID President: M. Roden
Chair: M. Roden (Germany), W. Waldhäusl (Austria)
A. Stirban (Germany):
Postprandial dysmetabolism and cardiovascular complications: therapeutic options
H. S. Willenberg (Germany):
Aldosterone and the metabolic syndrome
R. Lichiardopol (Romania):
Insulin resistance as an independent cardiovascular risk factor
16:30 – 17.00
Coffee break
17.00 – 18.30: Session II
Are we progressing in the therapy of diabetes?
Chair: R. Lehmann (Switzerland), P. Kempler (Hungary)
N. Schloot (Germany):
Type 1 diabetes: therapy and prevention
M. Roden (Germany):
Complex insulin therapy in type 2 diabetes
W. Waldhäusl (Austria):
Another view on diabetes therapy – how to optimize therapeutic outcome
18.30 – 19.30
Dinner educational
symposium sponsored
by Sanofi-Aventis
G. Bolli (Italy):
Benefits of insulin in type 2 diabetes mellitus
20.00
Welcome reception
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Program ştiinţific / Scientific Program
Day 2 : F r i day, S e p t 10 , 2 010
8.30 – 10.00: Session III
New therapeutic targets in diabetes
Chair: M. Graur (Romania), N. Schloot (Germany)
E. Standl (Germany):
Is type 2 diabetes indeed a CAD-equivalent? Evidence and therapeutic consequences
N. Lalic (Serbia):
Treatment of hypertension in diabetes: targets and how to reach them
H. Schatz (Germany):
New drugs for the management of hyperglycaemia
10.00 – 10.30
Coffee break
10.30-12.00: Session IV
The road from neuropathy to foot ulceration
Chair: R.Weitgasser (Austria), A. Stefanski (Poland)
R. Pop-Busui (USA):
Pathophysiology of diabetic neuropathy
V. Urbancic (Slovenia): The diabetic foot – predictors of outcome
I. A. Vereşiu (Romania):
Pathogenesis vs symptoms as therapeutic targets for diabetic neuropathy
12.00 – 12.30
Coffee break
12.30 – 13.30
Lunch educational
symposium sponsored by
Merck Sharp & Dohme
13.30 – 14.30
Lunch and Poster sessions
14.30 – 15.30: Session V
Oral presentations
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Chair: M. Moţa
I.A. Vereşiu:
Cost-efficacy with DPP4 inhibitors
C. Guja:
Cardiovascular effects of DPP4 inhibitors
Session 1 (posters 1 – 15):
Chair: W. Waldhäusl (Austria), S. Raptis (Greece)
Chair: E. Standl (Germany), H. Schatz (Germany)
Chair: T. Temelkova-Kurktschiev (Bulgaria), C. Bala (Romania)
Chair: V. Pirags (Latvia), M. Moţa (Romania)
M. Skrzypski, Thao Thu Le, P. Kaczmarek, E. Pruszynska-Oszmalek, P. Pietrzak,
D. Szczepankiewicz, M. Gierisch, A. Arafat, B. Wiedenmann, K. Nowak, M. Z. Strowski:
Orexin A regulates adipocyte function
I. R. Dinu, S. G. Popa, M. Mota, E. Mota, C. Stanciulescu, M. Ioana:
The association of the rs1049353 polymorphism of the CNR1 gene with
hyperleptinaemia in subjects with abdominal obesity
A. Muendlein, C. H. Saely, S. Geller-Rhomberg, G. Sonderegger, P. Rein, T. Winder, S. Beer, A. Vonbank, H. Drexel:
The presence of CAD significantly modulates the diabetes risk conferred by the
TCF7L2 rs7903146 variant
M. Zeyda, J. Huber, G. Prager, T. M. Stulnig: T cell subsets in human adipose tissue and correlations of their abundance with
inflammatory parameters in obesity
15.30 – 15.45
Break
15.45 – 16.45: Session VI
Oral presentations Chair : H. Schatz (Germany), A. Ştirban (Germany)
T. Märker, H. Sell, S. Famulla, P. Zilleßen, A. Glöde, J. Eckel, C. Habich:
The stress protein Hsp60: inflammatory and metabolic effects on human insulinsensitive cells
E. Kratz, J. M. Brix, F. Hoeller, H.-P. Kopp, G.-H. Schernthaner, G. Schernthaner:
Serum soluble glycoprotein 130 (sgp130) concentration is increased in morbid
obesity and declines after metabolic surgery
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www.diabetzaharat.info Diabet, Nutriţie, Risc Cardiometabolic, Numărul 2/2010
Scientific Program / Program ştiinţific
A. G. Tabak, M. Kivimaki, M. Carstensen, C. Herder, M. Jokela, E. J. Brunner, M. Roden,
M. Shipley, D. R. Witte:
Adiponectin trajectories preceding the development of type 2 diabetes mellitus –
13 year observation in the Whitehall II study
T. Milicic, N. M. Lalic, A. Jotic, V. S. Kostic, N. Covickovic Sternic, K. Lalic, L. Lukic,
M. Mijailovic, N. Rajkovic, M. Zamaklar, M. Macesic, J. P. Seferovic Mitrovic, S. Aleksic:
The analysis of insulin sensitivity and inflammatory markers levels in different subtypes of ischaemic stroke: comparison between type 2 diabetics and non-diabetics
16.45 – 17.00
Coffee break
17.00 – 18.00: Session VII
The road from metabolic syndrome to type 2 diabetes
Chair: H.S. Willenberg (Germany), V. Pirags (Latvia)
A. Stefanski (Poland):
Can we prevent type 2 diabetes?
T. Temelkova-Kurktschiev (Bulgaria):
Components of the MetS as predictors of diabetes
G. Roman (Romania):
Lifestyle intervention in the management of metabolic syndrome
18.00 – 19.00
Dinner educational
symposium sponsored
by Eli Lilly
Chair: I.A. Vereşiu
R. Lichiardopol (Romania):
Approval of an expected indication – exenatide plus TZDs
G. Roman (Romania):
Clinical benefits of exenatide therapy
20.00
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Gala dinner
Day 3 : S at u r day, S e p t 11, 2 010
8.00 – 8.30
8.30 – 9.30
9.30 – 10.15: Session VIII
State of the art lecture
FID board meeting
FID general assembly
R. Loos (UK):
Progress in the genetics of common obesity
10.15 – 10.45
Coffee break
10.45 – 12.00: Session VIII
Round table:
FID – Diabetes care, research and future career
development in Central
and Eastern Europe
Chair: M. Roden (Germany)
Panelists:
W. Waldhäusl (Austria) (FID President 1985 – 1995)
S. Raptis (Greece) (FID President 1995 – 1999)
E. Standl (Germany) (FID President 1999 – 2003)
H. Schatz (Germany) (FID President 2003 – 2009)
M. Roden (Germany) (FID President since 2009)
N. Lalic (Serbia)
V. Pirags (Latvia)
A. Stefanski (Poland)
A. Stirban (Germany)
C. Bala (Romania)
11.45 – 12.00
Coffee break
12.00 – 12.30
Closing ceremony and 26th FID Congress in Zürich announcement
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FID Meeting 2010
FID Meeting 2010, Cluj-Napoca, Romania
Oral Presentations
Oral 1
Orexin A regulates adipocyte
function
M. Skrzypski1,2, T. T. Le1, P. Kaczmarek2, E. Pruszynska-Oszmalek2, P. Pietrzak4, D. Szczepankiewicz2, M. Gierisch1, A. Arafat3, B. Wiedenmann1,
K. Nowak2, M. Z. Strowski1
1) Medizinische Klinik mit Schwerpunkt Hepatologie, Gastroenterologie & Interdisziplinäres Stoffwechsel-Zentrum/Endokrinologie und Diabetes
mellitus, Charité-Universitätsmedizin Berlin, Berlin,
Germany
2) Department of Animal Physiology and Biochemistry, Faculty of Animal Sciences, Poznań
University of Life Sciences, Poznań, Poland
3) Department of Endocrinology, Diabetes and
Nutrition, Charité-University Medicine Berlin,
Berlin, Germany
4) Department of Physiological Sciences, Faculty
of Veterinary Medicine, Warsaw University of Life
Sciences, Warsaw, Poland
AKT pathway. OXA increased cellular
ATP content, as well as lipid accumula
tion. OXA enhanced the lipogenesis and
reduced lipolysis. OXA increased adipo
nectin secretion and expression. OXA
increased the expression of PPARγ. The
effects of OXA on lipogenesis and adipo
nectin secretion were blocked by pharma
cological inhibitors of PPARγ activity and
by specific PPARγ siRNA.
Conclusions: In summary, our study
demonstrates that OXA PI3-kinase/AKTdependently stimulates glucose uptake in
adipocytes and that the evolving energy
is stored as lipids. OXA increases the ex
pression and secretion of adiponectin,
as well as lipogenesis through PPARγdependent mechanism. The effects of
OXA on the function of adipocytes may
be of clinical relevance in the pathophysi
ology of obesity and in peripheral insulin
resistance, the hallmark of type 2 diabetes
mellitus.
by the adipose tissue and controls various
metabolic functions. Several studies
indicated that rs1049353 (1359G/A)
polymorphism of the CNR1 gene is as
sociated with increased abdominal cir
cumference (AC).
The aim of our study was to investigate
the association between the rs1049353
polymorphism and increased leptin levels
in subjects with abdominal obesity (AO).
Materials and methods: The study
included 108 subjects with AO (AC
> 102 cm in men; AC > 88 cm in women)
and 80 subjects without AO. The groups
were divided in 2 subgroups: one with
high leptin levels (> 5,63 ng/ml for men;
> 11,09 ng/ml for women) and another
with normal leptin levels.
For all the subjects, anthropometric mea
surements were recorded, fasting plasma
leptin levels were determined using
ELISA immunoassay and the genotyp
ing of the rs1049353 polymorphism was
made using PCR technique. De Finetti’s
program was used for the statistical
analysis. The rs1049353 polymorphism
did not associate with AO (OR = 1.062,
p = 0.808).
Results: In the group with subjects with
AO: There was no deviation from Har
dy-Weinberg equilibrium of genotypes
distribution in both subgroups. The dif
ference of the allelic frequency indicated
that the G-allele seems to be protec
tive (OR = 0.419, CI = 0.211 – 0.830) and
the A-mutant allele seems to confer
risk for hyperleptinaemia (OR = 2.389,
CI = 1.204 – 4.738). Also, considering
G-allele as reference, the presence of
the AA genotype (OR = 37.08, p < 0.001)
and GA genotype (OR = 23.87, p = 0.003)
confers risk for hyperleptinaemia. In
order to increase the test sensitivity of
χ2, the Cochran-Armitage test was made.
The corrected values were ORcorrect
edG = 0.429 and ORcorrectedA = 5.847
(p = 0.008).
In the group with subjects without AO:
The A-mutant allele was not associated
with hyperleptinaemia.
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Background and aims: Orexin A (OXA)
plays a role in the regulation of food in
take and body metabolism. Dysfunction
of the orexin system is associated with
obesity and glucose intolerance. Recently,
orexin receptors were identified in human
adipocytes. Activation of orexin receptors
in adipocytes increased PPARγ2 expres
sion and reduced lipolysis. Here, we char
acterize the effects of OXA on glucose
uptake, lipid accumulation, adiponectin
gene expression, and secretion in adipo
cytes. We also describe the underlying
mechanism.
Materials and methods: We used isolated
primary rat adipocytes and differentiat
ed 3T3-L1 adipocytes. We studied the
effects of OXA on lipogenesis, lipolysis,
glucose uptake and ATP levels using bio
chemical assays, Western blots and im
munofluorescence. The effects of OXA
on adiponectin secretion and expression
were measured by RIA and Western blots.
Mechanisms of action were studied using
siRNA technique and pharmacological
inhibitors of crucial signaling pathways.
Results: OXA stimulated active glucose
uptake by translocating the glucose
transporter type 4 from plasma into the
plasma membrane via the PI3kinase/
Oral 2
The association of the rs1049353
polymorphism of the CNR1 gene
with hyperleptinaemia in subjects
with abdominal obesity
I.-R. Dinu1, S. G. Popa2, M. Mota2, E. Mota3,
C. Stanciulescu4, M. Ioana5
1) Clinical County Emergency Hospital, Diabetes,
Nutrition and Metabolic Diseases, Craiova,
Romania
2) University of Medicine and Pharmacy Craiova,
Diabetes, Nutrition and Metabolic Diseases,
Craiova, Romania
Nephrology, Craiova, Romania
Biochemistry, Craiova, Romania
Genetics, Craiova, Romania
Background and aims: The endocannabi
noid system (ECS) is involved in energy
balance and appetite stimulation. CNR1
is the gene encoding type 1 cannabinoid
receptor, implicated in the metabolic
functions of ECS. Leptin is secreted mainly
65
FID Meeting 2010
Conclusions: In conclusion, this study
indicates that in subjects with AO, the
presence of A-mutant allele of rs1049353
polymorphism in CNR1 gene is associated with hyperleptinaemia.
Oral 3
The presence of CAD significantly
modulates the diabetes risk
conferred by the TCF7L2 rs7903146
variant
A. Muendlein1,2,3, C. H. Saely1,2,3, S. Geller-Rhomberg1,2,3, G. Sonderegger1,2,3, P. Rein1,2,3, T. Winder1,2,3,
S. Beer1,2,3, A. Vonbank1,2,3, H. Drexel1,2,3,4
1) Vorarlberg Institute for Vascular Investigation
and Treatment (VIVIT), Feldkirch, Austria 2) Department of Medicine and Cardiology,
Academic Teaching Hospital Feldkirch, Feldkirch,
Austria 3) Private University of the Principality of Liechtenstein, Triesen, Liechtenstein 4) Drexel University College of Medicine, Philadelphia, PA, USA
OR = 1.59 [1.26 – 2.00]; p < 0.001), but not
in subjects who did not have significant
CAD (OR = 1.04 [0.77 – 1.40]; p = 0.807).
Variant rs7903146 was also significantly
associated with diabetes duration in individuals with CAD (7.9 ± 8.8, 8.9 ± 7.4
and 9.3 ± 6.8 years for the CC, CT, and
TT genotype, respectively; p = 0.018), but
not in patients without significant CAD
(p = 0.718). An interaction term CAD
x rs7903146 was significant (p = 0.018),
indicating a significantly stronger impact
of the polymorphism on T2DM risk in
patients with significant CAD than in
subjects without significant CAD.
Conclusion: We conclude that the
presence of CAD significantly modulates
the diabetes risk conferred by the TCF7L2
rs7903146 variant.
women and differentiated to adipocytes.
The release of adipokines after Hsp60
treatment (1 – 20 µg/ml) was measured by
multiplex beads assay. Insulin signalling
and MAP-kinase pathways were analyzed
by Westernblot. Specificity of Hsp60
binding to adipocytes was examined by
FACS.
Results: Unstimulated human (pre)adipocytes secreted measurable amounts of
TNFα, IL-6, IL-8, MCP-1 and RANTES.
Hsp60 led to increased secretion of
TNFα (up to 168-fold), IL-8 (up to
7-fold) and RANTES (up to 9-fold) from
preadipocytes, compared to control. For
mature adipocytes, Hsp60 stimulated
the secretion of TNFα (up to 21-fold),
IL-6 (up to 32-fold), IL-8 (up to 3-fold),
MCP-1 (up to 6-fold) and RANTES (up
to 8-fold) compared to unstimulated
cells. Hsp60 binding to adipocytes was
inhibitable (69 %) only by the unlabelled
ligand, thereby proving specificity of
Hsp60 binding.
Hsp60 induces insulin resistance on
the level of insulin-stimulated Akt and
GSK3 phosphorylation in human skeletal
muscle cells. To elucidate the processes
underlying Hsp60-mediated insulin resistance, stress signalling in skeletal muscle
cells was analyzed. Hsp60 increased the
phosphorylation of NF-κB, JNK and
ERK1/2 up to 2- to 3-fold over control.
Conclusions: We demonstrated for the
first time that Hsp60 treatment of human
(pre)adipocytes results in a dose- and differentiation-dependent release of various
proinflammatory mediators. In skeletal
muscle cells, Hsp60 activates proinflammatory signalling pathways and leads to
impaired insulin signalling. Therefore,
Hsp60 might be a factor underlying
adipose tissue inflammation and obesity-associated metabolic disorders.
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Background and aims: Genetic variant
rs7903146 in the transcription factor
7-like 2 (TCF7L2) gene has been consistently associated with type 2 diabetes
(T2DM) in several studies. It is unknown
whether it confers the same amount of
diabetes risk in patients with CAD as in
patients who do not have CAD.
Materials and methods: We therefore
performed genotyping of variant
rs7903146 in a large cohort of 1 650 consecutive Caucasian patients undergoing
coronary angiography for the evaluation
of established or suspected CAD. At angiography, significant CAD was diagnosed
in the presence of significant coronary
stenoses with lumen narrowing of ≥ 50 %.
The association between rs7903146 and
T2DM was evaluated in an additive
genetic model.
Results: Variant rs7903146 was significantly associated with the presence of
T2DM in the total study cohort (adjusted
odds ratio (OR) = 1.38 [1.15 – 1.65];
p < 0.001). Also, diabetes duration significantly (p = 0.024) increased from
the CC over the CT to the TT genotype
(7.7 ± 8.6, 8.1 ± 7.3 and 9.2 ± 6.8 years).
When patients with CAD (n = 950)
were analyzed separately from those
without significant CAD, the association between variant rs7903146 and
T2DM was strongly significant in
patients with significant CAD (adjusted
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Oral 4
The stress protein Hsp60:
inflammatory and metabolic effects
on human insulin-sensitive cells
T. Märker1, H. Sell2, S. Famulla2, P. Zilleßen1,
A. Glöde1, J. Eckel2, C. Habich1
1) Institute for Clinical Diabetology, 2) Institute for Clinical Biochemistry and
Pathobiochemistry, German Diabetes-Center,
Leibniz-Institute at the Heinrich Heine University
Duesseldorf, Germany
Background and aims: The autologous stress and heat shock protein 60
(Hsp60) induces the release of inflammatory mediators from adipose tissue
that represents an endocrine active organ
secreting a variety of bioactive proteins.
In the obese state, increased amounts
of proi nflammatory adipokines are
released by adipose tissue, that contribute to obesity-associated inflammation.
It is known, that obesity is a strong risk
factor for the development of insulin resistance, in which the crosstalk of adipose
tissue and skeletal muscle is involved.
Adipokines are important players in
this crosstalk causing local and systemic
effects. This study aimed to analyze the
inflammatory and metabolic effects of
Hsp60 on human insulin-sensitive cells,
i. e. adipocytes and skeletal muscle cells,
and to assess the role of Hsp60 in the development of insulin resistance.
Materials and methods: Preadipocytes
were isolated from subcutaneous adipose
tissue of lean or overweight healthy
Oral 5
Serum soluble glycoprotein 130
(sgp130) concentration is
increased in morbid obesity and
declines after metabolic surgery
E. Kratz¹, J. M. Brix¹, F. Hoellerl¹, H.-P. Kopp1,
G.-H. Schernthaner2, G. Schernthaner¹
1) Department of Internal Medicine I, Rudolf
stiftung Hospital Vienna, Vienna, Austria 2) Department of Internal Medicine II, Division of
Angiology, Medical University of Vienna, Vienna,
Austria
FID Meeting 2010
Background and aims: Glycoprotein
130 (gp130) is expressed on most cells
of the body and is present in the circulation in a soluble form: sgp130. Increased
sgp130 concentrations were recently
found in patients with polycystic ovarial
syndrome and hypertension. Activation
of gp130, the central signal transducer of
the interleukin-6 (IL-6)-related cytokines,
occurs in response to inflammation. The
soluble IL-6 receptor (sIL-6R) might
induce gp130 signalling and when
present leads to the sensitization of IL-6responsive cells towards the ligand. Up
to now sgp130 concentrations have not
been studied in morbid obesity (MO).
Therefore we investigated sgp130 levels,
sIL-6R and IL-6 levels in patients with
MO before and after metabolic surgery
(MS) compared to healthy controls (CO).
Materials and methods: We included 93
patients (mean age: 41 ± 11 years; mean
BMI: 45.9 ± 8.1 kg/m²) with MO in comparison with 28 controls (CO; mean age:
43 ± 14 years; mean BMI: 24.6 ± 2.7 kg/
m²). All patients were investigated before
and 2 years after metabolic surgery (MS).
Apart from weight and CV risk markers
(blood pressure, lipids), a glucose
tolerance test (75 g), renal and inflammation parameters were assessed. Sgp130
levels, soluble IL-6 receptor (sIL-6R) and
high sensitivity IL-6 (hsIl-6) levels were
assessed by a commercial ELISA. Statistics were calculated by SPSS.
Results: Patients with MO had significant higher sgp130 levels than CO:
202.3 ± 43.9 ng/ml vs. 192.2 ± 29.8 ng/
ml; p = 0.035. Sgp130 levels decreased
significantly after MS: 202.3 ± 43.9 ng/
ml vs. 184.6 ± 36.1 ng/ml; p < 0.001. In
a correlation analysis the delta sgp130
levels correlated with delta insulin
2-hour postprandial levels (r = 0.328;
p = 0.028), delta alanin-aminotransferase
(r = 0.291; p = 0.024) and delta aspartataminotransferase (r = 0.336; p = 0.008).
HsIL-6 levels dropped significantly after
MS: 3.7 ± 2.3 pg/ml vs. 2.6 ± 1.7 pg/ml;
p < 0.001. sIL-6R was lower in patients
with MO compared to CO (27.2 ± 7.8 ng/
ml vs. 31.4 ± 9.5 ng/ml; p = 0.023). Presurgery sgp130 levels correlated with presurgery: IL-6 (r = 0.309; p = 0.002), sIL-6R
(r = 0.186; p = 0.047), age (r = 0.206;
p = 0.033), Insulin 2-hour postprandial
(r = 0.277; p = 0.027) and alkaline phosphatase (r = 0.321; p = 0.001).
Conclusion: Patients with morbid obesity
have significantly higher sgp130 levels
and increased levels for IL-6 as well
as decreased levels of the soluble IL-6
receptor compared with CO. This is the
first study demonstrating a significant
decline of sgp130 after significant weight
loss in MO patients.
Oral 6
Adiponectin trajectories preceding
the development of type 2 diabetes
mellitus – 13 year observation in
the Whitehall II Study
A. G. Tabak1,2, M. Kivimaki1, M. Carstensen3,
C. Herder3, M. Jokela1, E. J. Brunner1, M. Roden3,4,
M. Shipley1, D. R. Witte1,5
1) Department of Epidemiology and Public
Health, University College London, UK
2) Semmelweis University Budapest, Hungary
3) Institute for Clinical Diabetology, German
Diabetes Center, Germany
4) University Hospital Duesseldorf, Duesseldorf,
Germany,
5) Steno Diabetes Center, Gentofte, Denmark
tin during the preceding 13 years based
on 755 serum samples in cases and 5 095
serum samples in non-cases.
Results: Log-transformed adiponectin
levels were already lower among cases
compared to non-cases 13 years before
year 0 (mean difference 0.28 [95 % CI
0.21 – 0.34] log2 mg/l). Log-adiponectin
levels decreased linearly throughout the
whole observation period in non-cases by
0.011 [95 % CI 0.006 – 0.017] log2 mg/l/
year from 9.3 [95 % CI 9.1 – 9.5] to 8.8
[95 % CI 8.6 – 9.0] mg/l. The decline in
adiponectin from 7.9 [95 % CI 7.5 – 8.3]
to 7.1 [95 % CI 6.8 – 7.4] mg/l among cases
was significantly steeper than that among
non-cases (mean difference in slopes
0.005 [95 % CI 0.001 – 0.010] log2 mg/l/
year). BMI explained a marked proportion of fasting adiponectin but had little
effect on the slope differences. In both
men and women, the decline in adiponectin was more pronounced in cases with an
early diagnosis of diabetes (i. e. < 52 years)
compared to cases with later diabetes
diagnosis. However, this faster decline
of adiponectin was dependent on BMI.
Conclusions: Adiponectin levels were
lower more than a decade before diabetes
manifestation and showed a steeper
decline in cases than in non-cases.
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Background and aims: Low levels of
serum adiponectin have repeatedly been
associated with the development of type 2
diabetes (T2D). To clarify the issues of
timing and causality, we investigated
trajectories of adiponectin before T2D
diagnosis (cases) compared to those who
did not develop diabetes during follow-up
(non-cases).
Materials and methods: This is a casecohort study within the Whitehall II
cohort with a total of 2 809 participants
without T2D at baseline (27.2 % women,
mean age at baseline 49.3 (SD 5.9) years
and average BMI 25.3 (SD 3.5) kg/m2).
During the follow-up period 335 individuals developed diabetes whereas 2 474
study participants remained diabetes-free.
Serum levels of adiponectin were
measured at up to three occasions (phase
3, the baseline: 1991 – 1994, phase 5:
1997 – 1999, and phase 7: 2003 – 2004).
Year 0 of the observation period was the
year of diabetes diagnosis for cases and
a randomly selected time point during
follow-up for non-cases. Adiponectin
levels were traced backwards to participants’ first participation in clinical
screening. Multilevel models adjusted
for age, sex and ethnicity were fitted to
the data to assess changes in adiponec-
Oral 7
T cell subsets in human adipose
tissue and correlations of their
abundance with inflammatory
parameters in obesity
M. Zeyda1, J. Huber1, G. Prager2, T. M. Stulnig1
1) Clinical Division of Endocrinology and
Metabolism, Department of Medicine III, Medical
University Vienna, Vienna, Austria
2) Department of Surgery, Medical University
Vienna, Vienna, Austria
Background and aims: Accumulation of
cytotoxic and T helper (Th)1 cells together
with a loss of regulatory T cells in gonadal
adipose tissue was recently shown to contribute to obesity-induced adipose tissue
inflammation and insulin resistance
in mice. Here, we aimed to investigate
abundance and proportion of T lymphocyte subpopulations in human adipose
tissue and correlations with systemic and
adipose tissue inflammation.
Materials and methods: Expression of
marker genes specific for pan-T cells
67
FID Meeting 2010
and T cell subsets in visceral and subcutaneous adipose tissue from highly obese
patients (n = 20) and lean to overweight
control subjects matched for age and sex.
Results: All T cell markers were significantly upregulated in obese adipose tissue
and correlated with adipose tissue inflammation. Proportions of cytotoxic T cells
and Th1 cells were unchanged whereas
those of regulatory T cells and Th2 were
increased in visceral adipose tissue from
obese compared to controls. Markers of
systemic and adipose tissue inflammation
positively correlated with visceral adipose
abundance of cytotoxic T cells and Th1
cells but also regulatory T cells within the
obese group.
Conclusions: Our data support a role
of T cells in human obesity-driven inflammation but argue against a loss of
protective regulatory T cells to contribute to adipose tissue inflammation in
obese patients as suggested by recently
published animal studies. Supported
by the Austrian National Bank (project
no. 12735) and the European Community’s 7th Framework Programme
(FP7/2007 – 2013) under grant agreement
no. 201608 (all to T. M. S).
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The analysis of insulin sensitivity
and inflammatory markers levels
in different subtypes of ischaemic
stroke: comparison between type 2
diabetics and non-diabetics.
T. Milicic1, N. M. Lalic1, A. Jotic1, V. S. Kostic2,
N. C. Sternic2, K. Lalic1, L. Lukic1, M. Mijailovic2,
N. Rajkovic1, M. Zamaklar1, M. Macesic1,
J. P. Seferovic Mitrovic1, S. Aleksic1
1) Clinic for Endocrinology, Diabetes and
Metabolic Diseases, Clinical Center of Serbia 2) Clinic for Neurology, Clinical Center of Serbia
Background and aims: Decreased insulin
sensitivity and inflammation play an
important role in the development and
progression of atherosclerosis, but their
influence in the pathogenesis of different
subtypes of ischaemic stroke have not
yet been clarified. Therefore, our study
was aimed to analyze the level of: [a]
insulin sensitivity (IS) and [b] inflammatory markers in patients with type 2
diabetes (T2D) with different subtypes
of ischaemic stroke: atherothrombotic
infarction (ATI) (group A1, N = 20), and
68
lacunar infarction (LI) (group A2, N = 14),
T2D without stroke (group B, N = 21),
non-diabetics with ATI or LI (group C1,
N = 24; C2, N = 13] and non-diabetics
without stroke (group D, N = 27).
Material and methods: ATI and LI were
confirmed on cranial computerized scan
or magnetic resonance imaging. Insulin
sensitivity was evaluated by using frequently sampled intravenous glucose
tolerance test (FSIGTT) together with
minimal model analysis and by determining insulin sensitivity index (Si). The
fibrinogen level was detected using spectrophotometry and hs-C reactive protein
(CRP) by ELISA method.
Results: The Si levels were significantly lower in A1 and A2 vs. B (1.02 ± 0.30,
1.3 ± 0.37 vs. 1.97 ± 0.97 min-1/mU/l
x 10 4; p < 0.05) and in C1 and C2
vs. D (3.51 ± 0.83, 3.80 ± 0.82 vs.
6.75 ± 0.71 min-1/mU/l x 104; p < 0.001),
while there was no difference between
groups A1 vs. A2 or C1 vs. C2. Fibrinogen and hs-CRP levels were significantly
higher in A1 and A2 vs. B (4.45 ± 0.30,
4.24 ± 0.83 vs. 3.25 ± 0.84 g/l; 17.86 ± 2.41,
14.80 ± 1.88 vs. 10.44 ± 0.1.90 g/l; p < 0.05)
and C1 and C2 vs. D [4.12 ± 0.35,
3.98 ± 0.58 vs. 3.27 ± 0.77 g/l; 7.38 ± 0.84,
6.60 ± 0.70 vs. 2.58 ± 0.38 g/l; p < 0.05),
but we could also not detect differences between A1 vs. A2 or C1 vs. C2. The
changes in Si significantly correlated with
fibrinogen and hs-CRP levels both in T2D
(r = -0.430; r = -0.362, p < 0.05) and nondiabetics (r = -0.416; r = -0.381, p < 0.05).
Conclusions: Decreased IS was associated
with higher fibrinogen and hs-CRP levels
both in T2D and non-diabetics with ATI
and LI. Our results implie that decreased
IS might exert an important part of its
atherogenic influence through activation
of the low-grade inflammation, irrespective of the subtype of ischaemic stroke.
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FID Meeting 2010
Poster Presentations
Poster 1
Toll-like receptor 4-dependent
inflammatory adipocyte activities
are controlled by immunologic and
metabolic factors
A. L. Reinbeck1, E. Gülden1, C. Habich1, V. Burkart1
1) German Diabetes Center, Institute for Clinical
Diabetology, Duesseldorf, Germany
Background and aims: The development
of insulin resistance and diabetes is associated with chronic systemic inflammation. Recent investigations indicate an
important role of adipocytes and their
mediators in the induction of these inflammatory conditions. Inflammatory
adipocyte activities depend on the expression of the Toll-like receptor 4 (TLR4),
the receptor for bacterial lipopolysaccharide (LPS), representing a strong proinflammatory signal. Recent observations
implicate that the development of inflammatory adipocyte functions strongly
depends on the conditions acting on adipocytes during their differentiation. Here,
we investigated, whether inflammatory
and/or metabolic factors affect the development of TLR4-dependent inflammatory adipocyte activities.
Materials and methods: Adipocytes of
the line 3T3-L1 were differentiated in the
presence of increasing concentrations of
LPS and glucose (Glc) (9 d). After another
7 d of cultivation in the presence of 1 g/l
Glc and the absence of LPS, the TLR4dependent responsiveness of the mature
adipocytes was investigated by exposure
to increasing concentrations of LPS
(24 h). The LPS-induced release of the
proinflammatory mediators monocyte
chemoattractant protein-1 (MCP-1) and
interleukin-6 (IL-6) was quantified by
ELISA.
Results: The differentiation of preadipocytes in the presence of LPS (0, 1, 100 ng/
ml) had no effect on the spontaneous
release of MCP-1 (14.4 ± 1.4 ng/ml) or
IL-6 (0.2 ± 0.1 ng/ml) by mature adipocytes, but significantly affected the LPSinduced release of the mediators. After
differentiation in the presence of 0, 1 or
100 ng/ml LPS, adipocytes exposed to
1 ng/ml LPS released decreasing amounts
of 54.7 ± 13.7 ng/ml, 35.7 ± 6.7 ng/ml and
18.8 ± 3.9 ng/ml MCP-1. In parallel, the
LPS-stimulated IL-6 release decreased
from 1.3 ± 0.2 ng/ml to 0.6 ± 0.1 ng/ml
in cultures of cells differentiated in the
presence of 1 or 100 ng/ml LPS. To assess
a possible effect of elevated Glc levels,
preadipocytes were differentiated in the
presence of 1, 2 or 4.5 g/l Glc. Increased
Glc concentrations did not affect the spontaneous release of MCP-1 (3.4 ± 1.5 ng/ml)
and IL-6 (0.1 ± 0.1 ng/ml) from mature
adipocytes, but significantly increased
their LPS-induced MCP-1 release from
4.1 ± 0.4 ng/ml (1 g/l Glc) to 8.8 ± 3.2 ng/
ml (2 g/l Glc) and 11.8 ± 4.1 ng/ml (4.5 g/l
Glc). In parallel, LPS-induced IL-6 release
increased from 0.2 ± 0.1 ng/ml (1 g/l
Glc) to 0.7 ± 0.1 ng/ml (2 g/l Glc) and
0.5 ± 0.1 ng/ml (4.5 g/l Glc).
Conclusions: Our results indicate that
immunologic and metabolic factors,
which act on (pre)adipocytes during differentiation, determine the proinflam
matory reactivity of mature adipocytes
by inducing prolonged alterations of their
TLR4-dependent responsiveness.
of patients were included in the study:
overweight and obese T2D (BMI ≥ 25 kg/
m2) (group A, n = 30), normal weight T2D
(BMI < 25 kg/m2) (group B, n = 30) and
normal weight, healthy subjects (group
C, n = 15).
Material and methods: Total adiponectin
(Mercodia, Sweden) and resistin (ALPCO
diagnostics, USA) levels were measured
by ELISA method. Levels of leptin were
determined by RIA method (Linco,
USA). Insulin levels were measured by
RIA method and insulin resistance was
calculated using homeostatic model assessment insulin resistance (HOMA-IR)
index.
Results: We found the lowest level of
adiponectin in group A, being significantly lower than in groups B and C (A:
3.6 ± 1.3; B: 4.9 ± 2.1; C: 7.3 ± 2.1 ng/ml, A
vs B and A vs C: p < 0.01, B vs C: p < 0.05).
However, the highest level of leptin was in
group A, being significantly higher than in
group B, but without significant difference
beetwen groups B and C (A: 11.11 ± 6.4; B:
6.39 ± 2.3; C: 5.8 ± 1.8 ng/ml, A vs B vs C:
p < 0.01; A vs B: p < 0.01, B vs C: p = NS).
Similarly, the highest level of resistin was
found in group A, being significantly
higher than in groups B and C (A: 9.2 ± 4.2;
B: 5.9 ± 2.2; C: 4.4 ± 1.71 pg/ml; A vs B vs C:
p < 0.01; A vs B: p < 0.01), but without differences between groups B and C. Simultaneously, insulin was significantly higher in
group A compared to groups B and C (A:
23.9 ± 10.1; B: 17.58 ± 6.7; C: 12.3 ± 3.9 mU/
ml; A vs B and A vs C: p < 0.01, B vs C:
p < 0.05). Regarding insulin resistance, we
found that HOMA-IR was significantly
higher in group A compared to groups
B and C, being higher in group B than
in group C (A: 7.6 ± 2.3; B: 5.4 ± 2.0; C:
2.4 ± 1.2; A vs B: p < 0.05, B vs C: p < 0.05).
The increased levels of resistin correlated
with HOMA-IR and insulin levels (r = 0.35,
p < 0.01 and r = 0.29, p < 0,01, respectively) and adiponectin negatively correlated
with HOMA-IR and insulin (r = -0.398,
p < 0.01 and r = -0.297, p < 0,01, respectively). However, we did not find a significant correlation between leptin and
insulin resistance.
Conclusion: Our results have demonstrated that the levels of adipocytokines
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Poster 2
Resistin, adiponectin and leptin
levels in type 2 diabetic patients:
correlation with obesity and insulin
resistance
N. Rajković1, M. Zamaklar1, K. Lalić1, N. MajkićSingh2, N. M. Lalić1, S. Singh1, L. Stošić1, A. Jotić1,
L. Lukić1, T. Miličić1
Metabolic Diseases, Clinical Center of Serbia 2) Institute for Medical Biochemistry, Belgrade,
Serbia
Background and aims: Adipose tissues
express and secrete cytokines which are
a molecular link between obesity, insulin
resistance and diabetes. Previous studies
have shown conflicting reports of the role
of adipocytokines especially of resistin
and leptin in obesity mediated type 2
diabetes (T2D). The aim of our study
was to investigate the levels of adiponectin, resistin and leptin and their correlation with obesity and insulin resistance in
patients with T2D. The following groups
FID Meeting 2010
were strongly influenced by obesity in
T2D patients. Decreased levels of adiponectin were linked with diabetes and
insulin resistance more than with obesity.
Our data also imply that increased levels
of resistin, but not leptin were strongly
influenced by insulin resistance and compensatory hyperinsulinaemia in obese
T2D patients.
Poster 3
Decreased insulin sensitivity and
lipid abnormalities in normogly
caemic patients with impaired
cognitive function: comparison
between Alzheimer’s disease and
mild cognitive impairment
M. Macesic1, N. M. Lalic1, V. S. Kostic2, A. Jotic1,
E. Stefanova2, K. Lalic1, T. Milicic1, L. Lukic1,
N. Rajkovic1, J. P. Seferovic Mitrovic1, S. Aleksic1
amount of glucose infused during steady
state period (80 – 120 min). PI levels were
determined by radioimmunoassay. Total
Ch, HDL-Ch, and triglyceride levels were
determined by using enzymatic method,
ApoAI, ApoAII, Lp(a), ApoB and ApoE
by using nephelometry. LDL-Ch was calculated using the formula of Friedewald.
Results: We found that total glucose
uptake was significantly lower in group A
vs B and it was lower in both of the groups
compared to C (M value: A: 6.30 ± 0.50;
B: 7.40 ± 0.51; C: 7.02 ± 0.22 mg/min/
kg, p < 0.01). In addition, basal PI levels
were higher in group A vs B, and they
were higher in those groups compared
to C (A: 14.46 ± 1.90; B: 12.00 ± 1.42; C:
7.23 ± 0.87 mU/l, p < 0.05). Moreover, the
levels of total Ch and LDL-Ch were significantly higher in group A and B vs C
(total Ch; A: 6.36 ± 0.12; B: 6.28 ± 0.25;
C: 5.60 ± 0.18; LDL-Ch: A: 4.30 ± 0.18;
B: 4.23 ± 0.21; C: 3.47 ± 0.16 mmol/l,
p < 0.01), while there was no difference
between groups A and B. The HDL-Ch
levels were significantly lower in group
A vs B and in both groups compared
to C (A: 1.19 ± 0.03; B: 1.32 ± 0.06; C:
1.46 ± 0,30 mmol/l, p < 0.01). Simultaneously, the levels of ApoAI were significantly lower in group A vs B and
also in both of the groups compared
to C (A: 1.48 ± 0.05; B: 1.62 ± 0.08; C:
2.00 ± 0,36 g/l, p < 0.01). There was no
difference in respect to levels of other
lipids between groups.
Conclusion: Our results have demonstrated that IS levels were decreased in
MCI, being intermediate between AD and
healthy controls, while the similar pattern
of changes was shown for HDL-Ch and
ApoAI levels. The results also imply that
decreases in IS are strongly associated
with the progression in the cognitive
function impairments, exerting pre
sumably this influence on the level of
HDL-Ch and ApoAI disturbances.
Metabolic Diseases, Clinical Center of Serbia,
Belgrade, Serbia
Background and aims: It has been demonstrated that proinflammatory cytokines
IL-6 and TNF-alpha are elevated in
various insulin-resistant states including
type 2 diabetes (T2D) and obesity. It has
also been described that the low grade
inflammation, associated with insulin
resistance, represents a well established
risk factor for hypertension. However the
role of insulin resistance and the proinflammatory cytokine levels in the development of hypertension in obesity and
T2D remains still unclear. We analyzed
the levels of (a) insulin resistance and
(b) proinflammatory cytokines in: (a)
obese T2D with hypertension (group A,
n = 30, BMI ≥ 25 kg/m2), (b) obese T2D
without hypertension (group B, n = 30,
BMI ≥ 25 kg/m2) and (c) nonobese healthy
controls (group C, n = 15, BMI < 25 kg/
m2).
Material and methods: Patients were
40 – 70 years old, matched by gender,
duration of diabetes, with optimal
glycaemic control (HbA1c 6.5 ± 0.6 %).
Hypertension was defined as systolic BP
≥ 140 mmHg and diastolic BP ≥ 90 mmHg,
measured by sphygmomanometer, or
by established use of antihypertensives.
Insulin sensitivity was measured with two
complementary methods: (a) homeostasis
model assessment of insulin resistance
(HOMA-IR) from fasting plasma glucose
and insulin levels, (b) a 75 g oral glucose
tolerance test using oral glucose insulin
sensitivity (OGIS) index. Plasma insulin
(PI) levels were measured by RIA method.
IL-6 and TNF-alpha levels were measured
by ELISA method.
Results: We have found significantly higher PI levels in group A (A:
31.05 ± 8.24 vs B: 17.23 ± 3.23 mU/ml,
p < 0.01), together with lower OGIS (A:
267 ± 35.42 vs B: 342.89 ± 32.0, p < 0.01) as
measurement of peripheral insulin resistance. However, there was no significant
difference in HOMA-IR level, reflecting hepatic insulin sensitivity between
obese T2D patients (A: 8.43 ± 4.69 vs B:
6.52 ± 3.04, p = NS) in respect to presence
of hypertension. The highest IL-6 levels
were in group A compared to groups B
and C, being significantly higher in group
A than in group B (A: 15.46 ± 5.15; B:
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2) Clinic for Neurology, Clinical Center of Serbia,
Belgrade, Serbia
Background and aims: Previous studies
have suggested that decreased insulin
sensitivity (IS) and dyslipidaemia might
influence the pathogenesis of Alzheimer’s disease (AD), while the role of IS
and lipid changes in the development of
mild cognitive impairment (MCI), the
intermediate cognitive disorder between
normal aging and AD, has not yet been
clarified. The study was aimed to analyze
the levels of (a) IS, (b) plasma insulin (PI)
and (c) lipid parameters: total cholesterol
(Ch), low-density (LDL) and high-density (HDL) Ch, triglycerides and apolipoproteins (ApoAI, ApoAII, ApoB, Lp(a)
and ApoE), in patients with AD, MCI,
and healthy controls.
Material and methods: We included
59 normoglycaemic patients with AD
(group A; BMI: 22.84 ± 0.81 kg/m2, age:
71.23 ± 7.50 years), 34 normoglycaemic patients with MCI (group B; BMI:
23.87 ± 0.57 kg/m2, age: 64.48 ± 10.59
years), and 27 matched controls (group C;
BMI: 24.32 ± 0.55 kg/m2, age: 60,22 ± 5,64
years). IS was evaluated by using 2-h euglycaemic hyperinsulinaemic clamp,
insulin infusion rate of 1 mU/kg bw/min,
glucose adjusted manually maintaining
euglycaemia (5 mmol/l). Total glucose
uptake (M value) was calculated on the
Poster 4
Hypertension in obese type 2
diabetes patients: relationship
to insulin resistance and
proinflammatory cytokine levels
L. Lukic1, N. M. Lalic1, A. Jotic1, T. Milicic1,
M. Zamaklarv, K. Lalic1, N. Rajkovic1, J. P. Seferovic
Mitrovic1, M. Macesic1, S. Aleksic1
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FID Meeting 2010
11.77 ± 6.09; C: 3.48 ± 1.48 pg/ml, A vs
B: p < 0.05; A vs C and B vs C: p < 0.01).
However, there were no significant differences in the level of TNF-alpha between
diabetics (A: 1.54 ± 0.41; B: 1.53 ± 0.42; C:
0.71 ± 0.30 pg/ml, A vs B p = NS; A vs C
and B vs C: p < 0.01). In addition, we found
a significant positive correlation between
both cytokines with PI and HOMA-IR
(IL-6: r = 0.456; r = 0.400, p < 0.01, TNFalpha: r = 0.474; r = 0.390, p < 0.01, respectively). Also, a negative correlation was
found between both cytokines and OGIS
(IL-6: r = -0.441; TNF-alpha: r = -0.607,
p < 0.01, respectively).
Conclusion: Our results demonstrate that
hypertension in obese T2D patients is associated with increases in both peripheral insulin resistance and proinflamma
tory cytokine levels. The results imply
that increases in IL-6 exhibit a stronger
influence compared to TNF-alpha levels
facilitating the presence of hypertension
in these patients.
Poster 5
Poster 6
Diabetic cardiomyopathy: cardiometabolic correlations and therapeutic implications
J. P. Seferović Mitrović1, N. M. Lalić1, P. M. Seferović2,
B. Vujisić Tešić2, A. Jotić1, A. D. Ristić2, T. Miličić1,
L. Lukić1, M. Macesic1, S. Aleksic1
Metabolic Diseases Clinical Centre of Serbia,
Belgrade, Serbia 2) Clinic for Cardiovascular Diseases, Clinical
Centre of Serbia, Belgrade, Serbia
Background and aims: To assess the prevalence of diabetic cardiomyopathy (DC),
an early complication of type 2 diabetes,
and to compare the metabolic and cardiovascular parameters in patients with and
without DC. In addition, the predictors
of DC and the correlations of the echocardiographic features with laboratory,
metabolic and therapeutic parameters
were investigated.
Materials and methods: The study cohort
included 78 type 2 diabetic patients
without hypertension and coronary artery
disease. They underwent high-resolution
transthoracic echocardiography including
tissue Doppler and exercise stress-echocardiography. Left ventricular diastolic
dysfunction (LVDD) was established, if
E/E’ ratio was ≥ 15 (early mitral valve
flow velocity/early diastolic lengthen
ing velocity) or, if E/E’ ratio ranged from
8 – 15 in the presence of increased values
of at least one of the following parameters:
left ventricular mass index, left ventricular volume index, E/A ratio, atrial fibrillation, NT-proBNP. Laboratory assessment
included metabolic analysis (parameters
of glycoregulation – HbA1c, lipid profile
and lipid subfractions), biomarkers of
inflammation, fibrinolysis, endothelial
function, NT-proBNP, proinflammatory cytokine and adiponectin. To analyse
insulin sensitivity, minimal model test
was performed in 28 patients. Statistical
analysis included descriptive and analytic
methods, as well as uni- and multiple
linear regression analysis.
Results: DC was diagnosed in 8/78
(10.3 %) patients. Patients with DC
were significantly older, had a higher
body surface area and used metformin
less frequently. HDL cholesterol and
apolipoprotein A1 were significantly
elevated in patients with DC. Univariant analysis identified older age, less
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Increased fatty liver index in obese
type 2 diabetes patients: an association both with insulin resistance
and hyperglycaemia
K. Lalic1, M. Zamaklar1, N. M. Lalic1, A. Jotic1,
N. Rajkovic1, L. Lukic1, T. Milicic1, S. Singh1, L. Stosic1
Metabolic Diseases, Belgrade, Serbia
Background and aims: It has been
recently shown that fatty liver index
(FLI), calculated from waist circumference, body mass index (BMI), triglyceride (Tg) and γGT levels, could be a
simple and accurate predictor of hepatic
steatosis (HS) in the general population, which in turn represents a high
risk marker for diabetes and cardiovascular diseases. The relationship between
development of HS, obesity and related
metabolic parameters (insulin resistance
(IR), fasting plasma glucose (FPG) and
cholesterol subfraction levels), both in
type 2 diabetics (T2D) and non-diabetic
subjects has not yet been elucidated. This
study was aimed to analyze (a) FLI levels,
(b) plasma insulin, FPG and IR levels and
(c) lipoprotein subfraction levels in the
following groups: (a) obese T2D patients
(group A, n = 30; BMI: 29.7 ± 0.7 kg/m2);
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(b) nonobese T2D patients (group B,
n = 20; BMI: 24.4 ± 0.3 kg/m2); (c) obese
non-diabetic patients (group C, n = 30;
BMI: 28.9 ± 0.5 kg/m2); and (d) non-obese
healthy subjects (group D, n = 20; BMI:
23.2 ± 0.4 kg/m2).
Material and methods: The presence of
HS was estimated using FLI (FLI > 60 =
likelihood > 78 % HS present; FLI < 20
= likelihood > 91 % HS absent). IR was
determined by homeostasis model assessment (HOMA-IR) calculated from
FPG levels (glucose oxidase method)
and insulin levels (RIA method). Total
cholesterol (Ch), HDL-Ch, LDL-Ch and
Tg levels were determined by enzymatic
methods.
Results: We found significantly higher
FLI levels in groups with obese patients
both with and without T2D (group A vs
B: 71.4 ± 4.1 vs 40.5 ± 7.9, p < 0.01; group
C vs D: 67.5 ± 4.2 vs 33.1 ± 5.7, p < 0.001).
Also, HOMA-IR, insulin and FPG values
were higher in group A vs B (HOMA-IR:
11.4 ± 1.9 vs 6.1 ± 0.6; insulin: 26.2 ± 3.2
vs 20.4 ± 2.3 mU/l; FPG: 9.1 ± 0.5 vs
6.9 ± 0.4 mmol/l; p < 0.05, respectively)
and in group C vs D (HOMA-IR: 4.9 ± 04
vs 3.1 ± 0.2, p < 0.05; insulin: 19.8 ± 1.8 vs
13.8 ± 1.0 mU/l, p < 0.01; FPG: 5.5 ± 0.1 vs
5.1 ± 0.1 mmol/l, p < 0.05). Simultaneously, only in T2D patients we found significantly lower levels of HDL-Ch in group
A vs B (1.12 ± 0.05 vs 1.36 ± 0.06 mmol/l;
p < 0.05) while we could not find significant differences in total Ch, LDL-Ch and
Tg levels between the groups. We also
found that in T2D patients FLI correlated
significantly only with FPG (r = 0.318,
p < 0.05) and HDL-Ch (r = -0.395,
p < 0.05), while in non-diabetics FLI correlated with HDL-Ch (r = -0.380; p < 0.05),
insulin (r = 0.486; p < 0.01) and HOMA-IR
(r = 0.547; p < 0.001). In contrast, when we
analyzed obese vs non-obese patients, irrespective of T2D, FLI correlated significantly with both HOMA-IR (r = 0.453,
p < 0.01) and insulin (r = 0.380, p < 0.05)
in obese patients only.
Conclusions: Our results showed that the
association between HS and obesity might
be based on increased IR and plasma
insulin and decreases in HDL-Ch levels
both in T2D and non-diabetics. Moreover,
our data imply that only in T2D patients
hyperglycaemia exerts an additional and
independent role in facilitating the development of HS.
FID Meeting 2010
frequent metformin therapy and apoli
poprotein A1 as statistically significant
predictors of DC. In addition, multiple
linear regression analysis demonstrated
that apolipoprotein A1 and less frequent
metformin therapy were independent
predictors of DC. Also, statistically sig
nificant correlations among E/E’ ratio and
age, HDL cholesterol, apolipoprotein A1
and metformin therapy were revealed.
Conclusion: This study demonstrated
that the prevalence of DC was 10.3 %,
when strict selection criteria were applied.
In our data, patients with DC were charac
terized by less frequent use of metformin
in previous treatment, as well as by signi
ficantly elevated HDL cholesterol and
apolipoprotein A1 levels. Furthermore,
less frequent use of metformin therapy
and higher apolipoprotein A1 levels were
recognized as independent predictors of
DC. Thus, our results suggest that the
development of DC is strongly influ
enced by two distinct metabolic impair
ments: 1) insulin resistance, which can be
modulated by metformin therapy, and 2)
changes in HDL cholesterol metabolism,
which lead to the increases of total HDL
cholesterol and apolipoprotein A1 levels
but simultaneously facilitate the develop
ment of the disease.
Poster 7
activator inhibitor 1 (PAI-1) and lipopro
tein subfraction (total cholesterol (Ch),
HDL-Ch, LDL-Ch and triglyceride)
levels, being important factors facilitating
atherosclerosis, in 34 patients with type
2 diabetes (T2D) and ischaemic stroke
(group A), 32 patients with T2D without
ischaemic stroke (group B); 34 non-dia
betics with ischaemic stroke (group C)
and 31 healthy controls (group D).
Material and methods: Diagnosis of
atherothrombotic infarction was done
by neurologist in accordance to clinical
features and brain imaging findings.
The patients with ischaemic stroke were
included in the study providing that
they did not show signs of cardioembol
ic cerebral infarction or coronary heart
disease. Insulin sensitivity was evaluated
by using frequently sampled intravenous
glucose tolerance test (FSIGTT) together
with minimal model analysis and by de
termining insulin sensitivity index (Si).
Plasma insulin (PI) levels were deter
mined by radioimmunossay, PAI-1 by
plasminogen chromogenic plasmin
substrate assay and lipid subfractions by
chromatography.
Results: We found that Si levels were
significantly lower in group A vs group
B (1.13 ± 0.21 vs 2.25 ± 0.92 min-1/mU/
lx104; p < 0.05) and in group C vs group D
(3.20 ± 0.54 vs 6.83 ± 0.76 min-1/mU/lx104;
p < 0.001). Simultaneously, we found that
PI, PAI-1 and LDL-Ch levels were higher
in group A vs group B (PI: 22.2 ± 2.9
vs 16.5 ± 1.4 mU/l; PAI-1: 5.9 ± 0.4 vs
4.2 ± 0.4 mU/l; LDL-Ch: 4.8 ± 0.3 vs
3.8 ± 0.3 mmol/l, p < 0.05) and in group
C vs group D (PI: 15.3 ± 2.5 vs 9.7 ± 1.3
mU/l; PAI-1: 4.7 ± 0.4 vs 2.5 ± 0.3 mU/l;
LDL-Ch: 3.7 ± 0.2 vs 2.8 ± 0.3 mU/l,
p < 0.01), without the differences in other
lipoprotein subfractions. Also, Si levels
correlated with PI, PAI-1 and LDL-Ch
levels both in T2D (r = 0.425, r = 0.377,
r = 0.361, respectively, p < 0.05) and nondiabetic subjects (r = 0.524, r = 0.470;
r = 0.455, respectively, p < 0.05).
Conclusion: Our results show that an
ischaemic stroke was strongly associated
with decreased insulin sensitivity, i. e.
insulin resistance, both in T2D and in
non-diabetics. Our results imply that
decreased insulin sensitivity levels in as
sociation with compensatory hyperinsu
linaemia, underlying the development
of the ischaemic stroke, might exert
their atherogenic influence through the
increased levels of PI, PAI-1 and LDL-Ch.
Poster 8
Adhesion molecules and endothelium-dependent vasodilation in
patients with metabolic syndrome
L. Umnova1, P. Tretjakovs1,2,3, A. Jurka1,2, I. Bormane2,
I. Miķelsone2, D. Reihmane2, G. Krieviņa2, K. Elksne2,3,
N. Fokina1, V. Pīrāgs1
1) Centre of Endocrinology, Pauls Stradins Clinical
University Hospital, Latvia
2) Institute of Experimental and Clinical Medicine,
University of Latvia, Latvia
3) Department of Human Physiology and Biochemistry, Riga Stradins University, Latvia
Background and aims: To evaluate the
relationships between insulin resistance
(IR), vascular cell adhesion molecule-1
(sVCAM-1), intercellular cell adhesion
molecule-1 (sICAM-1), sE-selectin, and
endothelium-dependent vasodilation
in obese metabolic syndrome (MetS)
patients who were grouped as having
type 2 diabetes mellitus (T2DM) or
both T2DM and coronary artery disease
(CAD), or neither.
Material and methods: The study included
34 patients with T2DM (D), 20 patients
with T2DM and CAD (DC), and 26
patients with MetS alone (M). 18 healthy
subjects were selected as controls (C). IR
was assessed by HOMA-IR method, but
serum sVCAM-1, sICAM-1, and sE-se
lectin levels were measured by xMAP
technology. Endothelium-dependent
vasodilation in the hand was assessed by
laser Doppler imaging with iontopho
retic application of 1 % acethylcholine
(LDI-Ach) solution.
Results: Serum levels of sVCAM-1,
sICAM-1, and sE-selectin in patients
with T2DM and CAD (p < 0.01) were
significantly higher than those in other
groups (p < 0.01), except for sICAM-1 in
the group with T2DM. All patient groups
showed significantly higher HOMA-IR
values compared to controls, and the
value of HOMA-IR in the group with
T2DM was higher than that in the group
of patients with MetS alone (D 5.77 ± 3.06
vs M 3.87 ± 1.86, p < 0.05), but did not
differ from the group of patients with
both T2DM and CAD. At the same time
sVCAM-1, sICAM-1, and sE-selectin
concentrations were significantly corre
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Decreased insulin sensitivity and
impairments in related metabolic
risk factors are associated with
occurrence of ischaemic stroke
both in type 2 diabetes and nondiabetic patients
A. Jotic1, N. M. Lalic1, V. S. Kostic2, N. Covickovic
Sternic2, K. Lalic1, T. Milicic1, L. Lukic1, M. Mijailovic2,
N. Rajkovic1, M. Zamaklar1, M. Macesic1,
J. P. Seferovic Mitrovic1, S. Aleksic1
Belgrade, Serbia
2) Clinic for Neurology, Clinical Center of Serbia,
Belgrade, Serbia
Background and aims: Decreased insulin
sensitivity (IS) plays an important role in
the pathogenesis of atherosclerosis, but
the role of IS and related metabolic risk
factors in occurrence of ischaemic stroke
has not yet been elucidated. Therefore the
study was aimed to analyze IS, together
with plasma insulin (PI), plasminogen
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FID Meeting 2010
lated with HOMA-IR indices (p < 0.0001).
Only D and DC patient groups showed
a significant and similar diminution in
LDI-Ach marker compared to controls
(p < 0.001). LDI-Ach values were significantly correlated with HOMA-IR indices,
sVCAM-1, sICAM-1, and sE-selectin
levels (p < 0.01).
Conclusions: Obese MetS patients with
T2DM have more apparent elevations
in serum levels of adhesion molecules
(sICAM-1, sVCAM-1, sE-selectin), simultaneously with both higher IR and lower
endothelium-dependent vasodilation than
those with MetS alone, but the presence of
CAD in these patients is associated with
more substantial changes in the markers
of endothelial dysfunction.
Poster 9
Material and methods: We enrolled 909
consecutive Caucasian patients, including
226 patients with type 2 diabetes (T2DM)
and 683 non-diabetic subjects who
were referred to coronary angiography
for the evaluation of stable coronary
artery disease (CAD). Elevated urinary
albumin excretion (UAE) was defined as
an urinary albumin to creatinine ratio
(ACR) ≥ 30 μg/mg; significant CAD was
diagnosed in the presence of coronary
artery lumen narrowing ≥ 50 %.
Results: The prevalence of significant CAD
was significantly higher in patients with an
elevated UAE than in those with normal
UAE (65.9 % vs 51.4 %; p < 0.001). Logistic
regression analysis adjusting for age,
gender, smoking, hypertension, LDL cholesterol, HDL cholesterol, CRP, BMI, use
of ace/angiotensin II antagonists, aspirin
and statins, as well as for the glomerular filtration rate (eGFR) and for T2DM
confirmed elevated UAE as a significant
predictor of angiographically determined
CAD (OR = 1.68 [1.15 – 2.44]; p = 0.007).
Similarly, the ACR was significantly associated with significant CAD when treated
as a continuous variable (standardized
adjusted OR = 1.45 [1.13 – 1.86]; p = 0.004).
The prevalence of elevated UAE was significantly higher in patients with T2DM
than in non-diabetic patients (38.9 % vs
18.0 %; p < 0.001). Like in the total study
cohort, the prevalence of significant CAD
was higher in patients with elevated UAE
than in those with normal UAE out both
in patients with diabetes (75.0 % vs 60.9 %;
p = 0.028) and in those without diabetes
(59.3 % vs 49.1 %; p = 0.040). Concordantly, the ACR proved significantly predictive of significant CAD both in patients
with T2DM (1.66 [1.01 – 2.74]; p = 0.045)
and in patients without diabetes (1.42
[1.05 – 1.92]; p = 0.023) in a fully adjusted
model.
Conclusion: An elevated UAE is strongly
associated with angiographically determined coronary atherosclerosis both in
patients with T2DM and in non-diabetic patients, independent of conventional cardiovascular risk factors and of the
eGFR.
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Agonist of growth hormone
releasing hormone as a potential
effector for survival and
proliferation of pancreatic islets
B. Ludwig1,2, C. G. Ziegler1, A. V. Schally3,?,
C. Richter1, A. Steffen1, N. Jabs1, R. H. Funk?,
M. D. Brendel1,2, N. L. Block?, M. Ehrhart-Bornstein1,
S. R. Bornstein1
1) University Hospital Carl Gustav Carus, Department of Medicine III, Dresden, Germany 2) Paul Langerhans Institute, Dresden, Germany 3) VA Medical Center and Departments of
Pathology and Medicine, Divisions of Endo
crinology and Hematology-Oncology, University
of Miami, Miller School of Medicine, Miami, FL,
USA 4) University Hospital Carl Gustav Carus, Institute
of Anatomy, Dresden, Germany 5) Department of Pathology, University of Miami,
Miller School of Medicine, Miami, FL, USA
Background and aims: Therapeutic strategies for transplantation of pancreatic islet
cells are urgently needed to expand β-cell
mass by stimulating islet cell proliferation and/or prolonging islet cell survival.
Control of the islets by different growth
factors provides a potential venue for augmenting β-cell mass.
Material, method and results: In the
present study, we demonstrated the expression of the biologically active splice
variant-1 (SV-1) of GHRH receptor in
rat insulinoma (INS-1) cells as well as
in rat and human pancreatic islets. In
studies in vitro of INS-1 cells, the GHRH
agonist JI-36 caused a significant increase
in cell proliferation and a reduction of
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cell apoptosis. JI-36 increased islet size
and glucose-stimulated insulin secretion
in isolated rat islets after 48 – 72 hours.
At the ultrastructural level, INS-1 cells
treated with agonist JI-36 revealed a
metabolic active stimulation state with
increased cytoplasm. Co-incubation
with the GHRH antagonist MIA-602
reversed the actions of the agonist JI-36,
indicating their specificity. In vivo, the
function of pancreatic islets was assessed
by transplantation of rat islets under the
kidney capsule of streptozotocin-induced
diabetic NOD-SCID mice. Islets treated
with GHRH agonist JI-36 were able to
achieve normoglycaemia earlier and
more consistently than untreated islets.
Furthermore, in contrast to diabetic
animals transplanted with untreated
islets, insulin response to an intraperitoneal glucose tolerance test (IPGTT)
in animals receiving islets treated with
agonist Jl-36 was comparable to that of
normal healthy mice.
Conclusion: In conclusion, our study
provides evidence that agonists of GHRH
represent a promising pharmacological
therapy aimed at promoting islet graft
growth and proliferation in diabetic
patients.
Poster 10
Albuminuria is associated with
angiographically determined
coronary atherosclerosis both in
patients with type 2 diabetes and in
non-diabetic individuals
C. Boehnel 1,3, P. Rein 1,2,3, C. H. Saely 1,2,3,
A. Vonbank1,2,3, S. Beer 1,2,3, V. Jankovic 1,3, J. Breuss 1,3,
L. Risch 1,2,3, H. Drexel 1,2,3,4
Background and aims: Albuminuria is
associated with atherothrombotic events
and all-cause mortality in patients with
diabetes as well as in non-diabetic individuals. However, it is not known,
whether albuminuria is associated with
directly visualised atherosclerosis in the
same manner.
P o s t e r 11
Cross-sectional study on the
prevalence of abnormal glucose
FID Meeting 2010
tolerance and its risk factors in the
adult population of Riga, Latvia
D. Misina1, N. C. Barengo2, L. Zarina3,
A. Derveniece1, J. Klovins4, V. Pirags3
1) Riga Stradins University, Latvia
2) University of Helsinki, Finland
3) Pauls Stradins Clinical University Hospital, Latvia
4) Latvian Biomedical Research and Study Centre,
Latvia
Background and aims: To assess the
current prevalence of abnormal glucose
tolerance (AGT), its risk factors and to
suggest the possible screening tool to
detect people with the high risk for AGT.
Material and methods: Study design:
A cross-sectional survey. Setting: The
practices of general practitioners in Riga,
Latvia.
A cross-sectional survey among the 45to 74-years old population randomly
selected from the registries of general
practitioners in Riga, Latvia was carried
out in 2008 – 2009. It consisted of the
questionnaire, objective measurements
such as height, weight, waist circumference, blood pressure as well as blood
samples of oral glucose tolerance test,
cholesterol and its fractions.
The Finnish diabetes risk score
(FINDRISC) questionnaire was tested as
a screening tool to detect the persons with
high risk for AGT.
Results: The information from 256
participants was included in the final
analysis. The prevalence of the AGT
was 27.3 % including type 2 diabetes of
15.2 %. Women with AGT had a worse
risk factor profile for T2D and cardio
vascular diseases compared to those
with normal glucose tolerance. No differences were found in risk factor profile
between men with and those without
AGT.
Overweight and obesity was detected in
72 % of men and 71 % of women. 6 % of
men and 8 % of women engaged in regular
physical activity. The fruit and vegetable
consumption was reaching up to 80 % in
both genders.
A high proportion of men and women
with more than 11 FINDRISC points had
undetected AGT.
Conclusions: Prevalence of AGT and
its risk factors were high in the Latvian
population.
The FINDRISC questionnaire can be used
locally in clinical practice to detect people
with AGT.
Poster 12
Diastolic dysfunction and cardiac
autonomic neuropathy in diabetes
mellitus
It is important to assess both heart rate
variability and diastolic dysfunction
in patients with long duration of DM,
even in the absence of cardiovascular
symptoms.
L. Poanta1, I. Damian1, D. L. Dumitrascu1
1) University of Medicine and Pharmacy Iuliu
Hatieganu, Cluj Napoca, Romania
Background and aims: Diabetic
autonomic neuropathy is a serious complication of diabetes mellitus, which worsens
the prognosis. Cardiac autonomic neuropathy (CAN) is also a serious but not
very well defined complication. The aim
of the study was to analyze the correlations between heart rate variability parameters and diastolic dysfunction in a
group of type 2 diabetes mellitus patients
without evidence of any cardiovascular
disease.
Material and methods: A group of 55
patients with type 2 diabetes mellitus
(DM) was selected, aged 62.8 ± 8.48
years. No subject had coronary artery
disease, hypertension, congestive heart
failure, or any evidence of clinical diabetic
complications. Left ventricle diameters
and diastolic function were evaluated
by Doppler echocardiography and CAN
was investigated using spectral analysis
of time and frequency domains from a
24 hours ECG recording (e. g. heart rate
variability).
Results: The disease duration was
9.19 ± 8.30 years. Mean fasting glucose
was 163.26 ± 50.38 mg/dl, and mean
HbA1c was 7.20 ± 1.59 %. There were
no significant differences regarding
the ejection fraction and left ventricle
diameters between DM group and control
group, but heart rate variability parameters were lower in DM patients (p < 0.05).
Also E/A ratio and isovolumic relaxing
time were significantly altered in DM
group (p < 0.05).
There are significant correlations between
diabetes duration and control (HbA1c
values), and the severity of the autonomic
dysfunction, as well as between the
presence of CAN (abnormal 24 hours
heart rate variability) and the parameters
of diastolic dysfunction. All patients in
our study had impaired relaxation pattern
of diastolic dysfunction.
Conclusion: In our study the presence of
CAN is associated with early diastolic dysfunction, without any clinical symptoms.
Poster 13
Endothelial dysfunction in young
people with metabolic syndrome
A. Gherbon1, L. Noveanu1, G. Mihalaş1
1) Department of Physiology – UMF ’V. Babeş‘
Timişoara, Romania
Background and aims: Endothelial dysfunction represents an early sign of arteriosclerosis. The metabolic syndrome is
related to a higher incidence of cardio
vascular diseases. Flow-mediated vasodilation represents a surrogate paramater
that mirrors cardiovascular risk. Its noninvasive nature makes it easy to use in
young people.
The aim of our study was to identify endothelial dysfunction using flow-mediated vasodilation (FMD) in young students
with metabolic syndrome, aged 20 ± 2
years.
Material and methods: Measurement of
FMD was performed at the brachial artery
in 22 subjects (14 male and 8 female).
Criteria for the metabolic syndrome were:
• abdominal circumference (above 80 cm
in female and above 94 cm in men),
• fasting glucose concentration above
100 mg/dl,
• HDL cholesterol below 40 mg/dl in male
and below 50 mg/dl in female,
• blood pressure above 130/85 mmHg,
• t riglyceride concentration above
150 mg/dl.
We also evaluated:
• lifestyle and level of stress (questionnaire method),
• lipid profile (total cholesterol, triglyce
rides, HDL cholesterol, LDL cholesterol),
• abdominal circumference and body
mass index (BMI).
Results: FMD values below 11 % were
found in all subjects with metabolic
syndrome, as opposed to healty controls.
FMD values below 11 % were associated
with higher levels of blood pressure
(female: p = 0.22, OR = 2.86, male:
p = 0.22, OR = 0.35) and triglyceride concentration (female: p = 0.33, OR = 0.38,
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male: p = 0.33, OR = 2.63) and also with
lower concentration of HDL cholesterol
in female (p = 0.6, OR = 0.71).
Conclusions: FMD evaluation in joung
subjects with metabolic syndrome
mirrors their increased cardiovascular
risk and is associated with cardiovascular
risk factors like elevated blood pressure
and high lipid levels.
P o s t e r 14
Evaluation of cardiovascular risk
factors in a large cohort of Austrian
patients with morbid obesity
F. Hoellerl¹, H.-P. Kopp¹, J. Maria Brix¹, G. H. Schernthaner2, S. Kriwanek³, G. Schernthaner¹
1) Department of Internal Medicine I, Rudolfstiftung Hospital Vienna, Austria 2) Department of Internal Medicine II, Division of
Angiology, Medical University of Vienna, Austria 3) Department of Surgery, Rudolfstiftung Hospital
Vienna, Austria
dl, p = 0.016, and triglycerides levels
212 ± 137 vs 145 ± 74 mg/dl, p < 0.001,
and were significantly higher in the DM
group, whereas HDL-cholesterol (chol)
(46 ± 12 vs 50 ± 14 mg/dl, p = 0.001) and
LDL-chol (109 ± 39 vs 120 ± 35 mg/dl,
p = 0.001) levels were lower in patients
with DM versus those without DM.
HOMA-IR was elevated in both groups,
but significantly higher in the DM group
(11.6 ± 10.9 vs 4.8 ± 3.5, p < 0.001). An
increase in albumin excretion rate (AER)
was noted in 32.1 % of the patients with
DM and in 15.8 % of non-DM patients
(χ² = 0.001). BMI, CRP and total chol
levels were not significantly different
between the groups. Remarkably, the
DM patients were 10 years older, indicating the longer exposure to morbid
obesity may induce diabetes at the same
level of BMI. In the longitudinal observation HbA1c levels decreased dramatically in the DM patients (7.5 ± 1.5 % vs
5.7 ± 0.7 %, p < 0.001), but showed also
an improvement in the non-DM group
(5.5 ± 0.4 % vs 5.2 ± 0.4 %, p < 0.001).
Conclusion: In the very large cohort of
Austrian patients with MO, those with
DM have a much higher CV risk profile
compared with non-DM. These findings
may explain why outcome studies show
the greatest benefit in DM patients, who
should be the preferred candidates for BS
due to the limited capacities.
Material and methods: We recorded
vascular events over a mean period of
7.2 years in 491 consecutive statin-treated patients with angiographically proven
stable CAD, covering 3 518 patient years.
Results: In the total population, low HDL
cholesterol (standardized adjusted HR
0.80 [0.67 – 0.94]; p = 0.009), low apolipoprotein A1 (0.84 [0.72 – 0.98]; p = 0.022),
a small LDL particle diameter (0.84
[0.72 – 0.98]; p = 0.023), and high triglycerides (1.18 [1.04 – 1.35]; p = 0.013)
predicted vascular events, but not total
cholesterol, LDL cholesterol, or apolipoprotein B. Factor analysis in the lipid
profiles of our patients revealed an HDLrelated factor and an LDL-related factor.
Concordant with the results for individual lipid parameters, the HDL-related
factor (0.76 [0.65 – 0.90]; p = 0.001), but
not the LDL-related factor (p = 0.644)
predicted vascular events. Patients with
type 2 diabetes (T2DM; n = 116) were at
a higher vascular risk than non-diabetic
subjects (52.6 % vs 36.8 %; p = 0.002), and
like in the total population the HDL-related factor (0.63 [0.49 – 0.81]; p < 0.001),
but not the LDL-related factor (p = 0.976)
predicted vascular risk in diabetic
patients.
Conclusion: The pattern of low HDL
cholesterol, low apolipoprotein A1,
small LDL particles, and high triglyce
rides drives vascular risk in statin-treated
coronary patients, particularly in those
with T2DM.
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Background and aims: Outcome
studies in patients with morbid obesity
(MO) have shown that diabetic patients
have the greatest benefit from weight
reduction induced by bariatric surgery
(BS). Therefore it was of interest to study a
variety of cardiovascular (CV) risk factors
in a very large group of Austrian patients
with MO (n = 1 015) presenting with or
without diabetes mellitus (DM).
Material and methods: In 1 015 patients
with MO (mean age was 40 ± 12 years, 800
females, 215 males), DM was diagnosed
(ADA criteria) in 178 patients (17.6 %;
mean HbA1c 7.7 ± 1.7 %). In the non-DM
patients, a 75 g oral glucose tolerance test
was performed; 25.4 % presented with
impaired (IGT) and 57.0 % with normal
glucose tolerance. HOMA-insulin resistance (IR) was calculated. In addition, 176
patients were followed up 2 years after
BS, of whom 26 % (n = 42) were diabetic.
CV risk factors, demographic, renal and
inflammation parameters were assessed.
All patients collected urine on 3 consecutive days over 24 hours to determine albuminuria.
Results: The following differences between the groups were determined (each DM vs non-DM): systolic
blood pressure (BP) 148 ± 19 vs
141 ± 15 mmHg, p < 0.001; diastolic BP
90 ± 12 vs 88 ± 10 mmHg, p = 0.036; creatinine 0.85 ± 0.29 vs 0.79 ± 0.15 mg/
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Poster 15
Factors predicting cardiovascular
events in statin-treated diabetic
and non-diabetic coronary
patients: a prospective cohort
study
H. Drexel 1,2,3,4, S. Greber 1,2,3, T. Gansch 1,2,3, P. Rein 1,2,3,
A. Vonbank 1,2,3, C. H. Saely 1,2,3
Background and aims: We aimed at
identifying which lipid factors drive
vascular risk in statin treated patients with
coronary artery disease (CAD).
Post e r 16
High motivation for lifestyle modification among Bulgarian urban
population: the Sofia Lifestyle (SLS)
Study
I. Bonova1, T. Stefanov2, A. Vekova2, T. TemelkovaKurktschiev2
1) Unit Sport Pedagogy, International Scientific Institute, National Sports Academy, Sofia, Bulgaria 2) Medicobiological Unit, International Scientific
Institute, National Sports Academy, Sofia, Bulgaria
Background and aims: At present,
various type 2 diabetes (T2DM) prevention strategies targeting increase in
the level of physical activity and modification of nutritional habits are being
developed and promoted among the
society. Without the motivated, conscious
participation of the general population,
FID Meeting 2010
these strategies may, however, appear unsuccessful. In the present study, we aimed
at investigating the self-perception of
nutritional habits and level of physical
activity (PA) as well as the motivation for
lifestyle modification among the citizens
of Sofia, Bulgaria.
Material and methods: A total number
of 511 randomly chosen participants
completed a validated questionnaire concerning age, height, body weight, history
of type 2 diabetes, arterial hypertension,
high cholesterol levels, and cardiovascular
disease (CVD), self-perception of nutritional habits and PA, and motivation for a
lifestyle change. The Baecke PA questionnaire distinguishing three components of
daily PA (sport, leisure time and occupational PA) and the Three Factor Eating
Questionnaire were also completed.
Results: Mean age of the participants was
37.7 ± 16 years and mean body mass index
(BMI) 24.7 ± 4.6 kg/m² (mean ± SD). A total
of 43.3 % of the participants were smokers,
26 % were overweight and 19 % obese,
14.1 % had history of hypertension, 9.8 %
of dyslipidaemia, 3 % of T2DM, and 5 % of
CVD. 58 % of the respondents perceived
their nutritional habits as unhealthy and
66.7 % considered their daily physical
activity as insufficient. According to the
results from the Baecke questionnaire the
level of physical inactivity among participants was even greater since 81 %, 78 % and
68.5 % of them reported physical activity
below the average value of 3 for work,
sport, and leisure time indices, respectively. Remarkably, 87.5 % (89.6 % vs 85.7 %,
men vs women, respectively) of the participants were willing to modify their way of
life in order to improve their health status
and wellbeing. Moreover, 97.3 % (96.1 %
vs 96.7 %, men vs women, respectively) of
them were highly motivated to increase
their physical activity level and to limit
their food intake.
Conclusions: In the present study we
demonstrated that the citizens of Sofia,
Bulgaria, are highly motivated to acquire
a healthier lifestyle in order to enhance
health and improve wellbeing. Since the
primary means of choice are engagement
in regular physical activity and modification of nutritional habits, our results may
indicate that community-based prevention programs are urgently awaited and
will show promising outcomes within this
population.
Post e r 17
High thrombin generation is
associated with macrovascular
disease in type 2 diabetes patients
with nephropathy
L. Ay1, F. Hoellerl1,3, J.-M. Brix1, C. Ay2, S. Koder2,
G.-H. Schernthaner3, I. Pabinger2, G. Schernthaner1
1) Department of Internal Medicine I, Rudolfstiftung
Hospital Vienna, Austria
2) Division of Haematology and Haemostaseology,
Department of Internal Medicine I, Medical University of Vienna, Austria
3) Division of Angiology, Department of Internal
Medicine II, Medical University of Vienna, Vienna,
Austria
Background and aims: It is well known
that albuminuria is a powerful prognostic
indicator of cardiovascular morbidity and
mortality in patients with type 2 diabetes
mellitus (T2DM). Laboratory tests which
globally measure the overall coagulation
potential might be useful to elucidate the
risk for cardiovascular disease in T2DM
with diabetic nephropathy.
Material and methods: In our crosssectional study we measured thrombin
generation (TG), a key process in haemostasis and a very promising tool to detect
the individual’s coagulation potential, in
different stages of renal failure (normo-,
micro-, and macroalbuminuria) in
T2DM with and without macrovascular disease. The thrombin generation
assay (Technothrombin TGA, Technoclone, Vienna, Austria) was performed
and the thrombin generation (TG) curve
(including the lag phase, peak thrombin
and area under the curve (AUC), representing the endogenous thrombin
potential) was analyzed. Statistical
analyses were done with ANOVA and
students’ unpaired t-test.
Results: A total of 161 patients with
T2DM (age: 67 ± 11 years (mean ± STD),
61 (39 %) female) and normo,- micro-,
or macroalbuminuria were investigated.
90 patients had normoalbuminuria, 40
microalbuminuria, and 31 macroalbuminuria. The AUC between the groups of
patients with normo-, micro-, and macroalbuminuria was statistically significant different (3 297 (2 795; 3 762) vs 3 209
(2 338; 3 643) vs 3 724 (3 252; 4 222) nM
thrombin; p = 0.005). T2DM patients
with macrovascular disease (n = 117), i. e.
coronary heart disease, peripheral arterial
vascular disease or stroke, had signifi-
cantly shorter lag phase (12 (9; 17) vs 20
(16; 25) seconds; p < 0,001), significantly
higher peak thrombin (233 (132; 338) vs
110 (82; 150) nM; p < 0,001) and significantly higher AUC (3 461 (2 991; 3 869) vs
3 091 (2 384; 3 619) nM thrombin; p < 0.01)
than T2DM patients without macrovascular disease (n = 44), indicating an earlier
and higher thrombin generation.
Conclusion: Our results support the hypothesis that TG may be involved in the
pathogenesis of macrovascular disease in
diabetic nephropathy. For the first time,
we could show that patients with T2DM
in different stages of diabetic nephropathy had disturbances in propagation of
thrombin, which may be a link between
cardiovascular disease and diabetic nephropathy.
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Poster 18
Hsp60-induced release of inflammatory mediators by adipocytes
of the New Zealand Obese Mice
is mediated by members of the
MAP-kinase family and NFκB
J. Kriebel1, T. Märker1, V. Burkart1, C. Habich1
1) Institute for Clinical Diabetology, German
Diabetes-Center, Leibniz-Institute at the HeinrichHeine-University Duesseldorf, Germany
Background and aims: Adipocytes
and their mediators are known to play
central roles in the development of the
metabolic syndrome and in the pathogenesis of diabetes. Recent studies with New
Zealand Obese (NZO) mice, a model of
the metabolic syndrome, identified heat
shock protein 60 (Hsp60) as an endogenous stress signal with adipocyte stimulating capacity. Hsp60 induces the release
of proinflammatory mediators from adipocytes in a receptor-mediated way. For
the development of intervention strategies
aiming at the modulation of adipocytedriven proinflammatory processes, our
present study was designed to identify
key components of signalling pathways
involved in the Hsp60-induced release of
inflammatory adipocyte mediators.
Materials and methods: Hsp60-mediated activation of the MAP-kinases p38,
ERK1/2, JNK and the transcription factor
NFκB was analyzed in NZO mouse-de
rived adipocytes. The involvement of these
signalling proteins in the Hsp60-induced
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release of the proinflammatory mediators
IL-6, KC and MCP-1 was investigated by
applying specific inhibitors and measured
by multiplex beads analyses.
Results: Hsp60 activates members of the
MAP-kinase family and NFκB in primary
adipocytes. Hsp60 (10 µg/ml) slightly
activated ERK1/2 phosphorylation in
mature adipocytes (1.4 ± 0.4-fold). JNK
was weakly activated in (pre)adipocytes
up to 2.2 ± 1.2-fold. No activation of p38
was observed. NFκB activation was significantly increased (up to 2.6 ± 0.9-fold)
in Hsp60-exposed cells. The ERK1/2
inhibitor PD98059 slightly suppressed
MCP-1 release in preadipoc ytes from
5.3 ± 2.0 ng/ml to 3.6 ± 1.4 ng/ml, whereas
in adipocytes MCP-1 release was significantly reduced from 8.3 ± 5.1 ng/ml to
1.9 ± 2.3 ng/ml. IL-6 and KC release was
unaffected. JNK inhibition by SP600125
caused a significant, dose-dependent inhibition of KC release from adipocytes
and of MCP-1 release from preadipocytes
and adipocytes. NFκB inhibition by SN50
resulted in a maturation-independent, significant, dose-dependent reduction of IL-6
(up to 99.9 % inhibition), KC (up to 91.8 %
inhibition) and MCP-1 (up to 94.1 % inhibition) secretion from adipocytes.
Conclusions: We could show that ERK1/2
is involved in the Hsp60-induced release
of MCP-1 from adipocytes. JNK takes
part in the release of KC in adipocytes
and MCP-1 independent of the maturation state. The transcription factor NFκB
is involved in the IL-6, KC and MCP-1
release in a maturation-independent
manner. Our findings will contribute to
identify components of the intracellular
signalling cascades as potential targets for
the modulation of diabetes-associated inflammatory adipocyte activities induced
by endogenous stress signals.
sistance and diabetes very often have low
testosterone level.
Aims: To analyze data about hypogonadism association with diabetes and
adiposity among men with diabetes
in Pauls Stradins Clinical University
Hospital, Department of Endocrinology.
Materials and methods: We analyzed
44 men, aged 19 – 68 years, with type 1
diabetes in 14 patients and type 2 diabetes
in 30 patients. All men with acute health
problems were excluded. We measured
total testosterone, HbA1c levels, BMI and
waist circumference. Two questionnaires
were used to collect information about
clinical symptoms of hypogonadism or
erectyle disfunction – ‘Androgen Deficiency in Aging Men (ADAM) questionnaire’ and ‘5-Item Version of the International Index of Erectile Dysfunction
(IIEF-5)’. Data were analyzed with MS
Excel and SPSS 16.0 programs.
Results: 7 patients (15.9 %) had a level
of total testosterone between 2.31 and
3.46 ng/ml, 6 patients (13.6 %) had a level
of total testosterone ≤ 2.31 ng.ml. There
was a statistically significant negative
correlation between age and testosterone level: r = -0.5, p < 0.001 (when age
increasing for 1 year, testosterone level
decrease 0.127 ng/ml per year; p < 0.001),
body mass index and testosterone level:
r = -0.6, p < 0.001 (when BMI increases
for 1 unit, testosterone level decreases
0.249 ng/ml per year, p < 0.001), waist
circumference and testosterone level:
r = -0.7, p < 0.001 (when waist circumference increases for 1 cm, testosterone level
decreases 0.083 ng/ml per year, p < 0.001,
independently from age). It was a difference of 5.11 ng/ml in testosterone level
(p < 0.001) between patients with type 1
and type 2 diabetes, adjusted for age. We
did not find statistically significant correlation between total testosterone and
HbA1c, r = -0.01, p < 0.9, total testosterone and duration of diabetes in years,
r = 0.2, p < 0.1, total testosterone and hypogonadism/erectile dysfunction clinical
symptoms. ADAM questionnaire showed
that 34 (80,9 %) of patients could have
hypogonadism.
Conclusions: The testosterone level is
strongly associated with adiposity in men
with diabetes. Influence of glucose level
or duration of diabetes is less important
than adiposity on decrease of testosterone
level. Clinical symptoms of hypogonad-
ism and erectyle dysfunction are multifactorial in this group and do not correlate
with testosterone level.
Poster 20
Impact of physical activity and
eating behavior on obesity and
type 2 diabetes: Sofia Lifestyle
(SLS) Study
T. Stefanov1, A. Vekova1, I. Bonova2, T. TemelkovaKurktschiev1
1) Medicobiological Unit, International Scientific
Institute, National Sports Academy, Sofia, Bulgaria 2) Unit Sport Pedagogy, International Scientific
Background and aims: Physical inactivity
and food overconsumption – two typical
features of the contemporary western way
of life – are considered as main contributors to the epidemic of obesity and type
2 diabetes mellitus (T2DM). The aim
of the present study was to investigate
the joint association of physical activity
(PA) during leisure time and uncontrolled
eating behavior with obesity and history
of T2DM among the citizens of Sofia,
Bulgaria.
completed a validated questionnaire concerning age, height, body weight, history
of T2DM, arterial hypertension, high cholesterol levels, and cardiovascular disease
(CVD), self-perception of nutritional
habits and physical activity, and motivation for a lifestyle change. The Baecke PA
questionnaire and the Three Factor Eating
Questionnaire were also completed.
(BMI) 24.7 ± 4.6 kg/m² (mean ± SD). 55 %
had normal body weight, 26 % were overweight, 19 % obese; and 3 % had history
of T2DM. The prevalence of T2DM was
significantly correlated with both leisure
time PA (p = 0.016; r = -0.186) and uncontrolled eating behavior (p = 0.04;
r = 0.159). BMI was found to be significantly higher among subjects in the
lowest when compared to subjects in the
middle (27.7 ± 6.9 vs 24.5 ± 4.5 kg/m²;
p = 0.002) and in the highest tertile of
leisure time PA (27.7 ± 6.9 vs 23.8 ± 4.9 kg/
m2; p < 0.001). A statistically significant
difference with respect to BMI was also
observed between the lowest and the
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Poster 19
Hypogonadism, adiposity and
diabetes mellitus in men
I. Lase1,2, I. Balcere1,2, I. Strele1,2
1) Pauls Stradins Clinical University Hospital, Riga, Latvia 2) Riga Stradins University, Riga, Latvia
Background: There is an increasing prevalence of adiposity and diabetes type 2 in
the world. Men with adiposity, insulin re78
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middle (24.2 ± 5.1 vs 26.7 ± 6 kg/m²;
p = 0.017) as well as between the middle
and the highest (24.7 ± 5.7 vs 26.7 ± 6 kg/
m²; p = 0.04) tertile of uncontrolled
eating behavior. The highest BMI was
observed among individuals that were
physically least active and had highest
uncontrolled eating behavior scores. In
a multiple regression analysis both uncontrolled eating behavior and leisure
time PA were independently associated
with BMI (β = 0.268, 95 % CI 0.16 – 0.42,
p < 0.001, and β = -0.159, -2.14 – -0.212,
p = 0.017).
Conclusions: We observed a strong association of leisure time physical activity
and uncontrolled eating behavior with
both BMI and prevalence of T2DM. Uncontrolled eating behavior seems to have
a greater impact on BMI than leisure
time PA. Neither of these factors should,
however, be underestimated when obesity
and T2DM prevention strategies are implemented.
Poster 21
lin resistance (IR) was calculated. Apart
from demographic and CV risk factors,
renal and inflammation parameters were
assessed. All patients collected urine on
3 consecutive days over 24 hours for the
determination of albuminuria.
Results: Gender differences in MO patients
were the following (each female vs male):
systolic blood pressure (BP) 141 ± 15 vs
148 ± 19 mmHg, p = 0.002; diastolic BP
89 ± 10 vs 91 ± 13 mmHg, p = 0.014; Chol/
HDL ratio 4.1 ± 1.2 vs 4.9 ± 1.3, p < 0.001;
triglycerides 156 ± 85 vs 195 ± 128 mg/dl,
p < 0.001; HDL-chol 51 ± 14 vs 42 ± 9 mg/
dl, p < 0.001; eGFR (MDRD) 104 ± 26
vs 93 ± 21 ml/min/1,73 m2, p < 0.001;
HOMA 5.7 ± 4.6 vs 8.9 ± 8.9, p < 0.001.
Women and men did not differ in age
(40 ± 12 vs 39 ± 12 years, p = 0.393), but
there were significant differences in BMI
(43.5 ± 9.7 vs 45.5 ± 9.2 kg/m2, p = 0.008).
Therefore we adjusted our results for
BMI. An increase in albumin excretion
rate (AER) was noted in 34.8 % of men
and in 17.2 % of women (χ² = 23.240,
p < 0.001). 50.3 % (n = 99) of men had a
normal glucose tolerance (NGT), 21.3 %
(n = 42) had an impaired glucose tolerance
(IGT), and 28.4 % (n = 56) had diabetes,
compared with 57.6 % (n = 416) of women
had NGT, 25.5 % (n = 184) had IGT and
16.9 % (n = 122) were diabetic (χ² = 18.934,
p = 0.001).
Conclusion: This study demonstrated
that MO men have a higher risk profile
than MO women suggesting that MO
men should be favored candidates for
bariatric surgery.
patients with morbid obesity (MO) in
relation to their metabolic state.
Material and methods: 745 MO patients
(77.8 % women, mean age 39.5 ± 12.0
years) were included in a cross-sectional study compared to 91 healthy controls
(63.8 % women, mean age 45.4 ± 14.0 years,
mean BMI 25.6 ± 4.4 kg/m²). 130 patients
with MO (mean BMI 44.9 ± 5.9 kg/m²)
were included in our longitudinal study
and were analysed before and two years
after bariatric surgery. Apart from serum
magnesium levels, weight, a glucose
tolerance test and standard laboratory
parameters were assessed.
Results: Patients with MO had significantly lower magnesium levels compared
with healthy controls (0.84 ± 0.09 mmol/l
vs 0.92 ± 0.06 mmol/l; p < 0.001).
Magnesium levels were significantly
lower in patients with T2D compared to
patients with normal glucose tolerance
(NGT) before surgery (0.77 ± 0.08
vs 0.85 ± 0.07 mg/dl; p < 0.001). Additionally we found a significant difference in the change of magnesium
between both groups after surgery
(T2D vs NGT -0.09 ± 0.09 mmol/l vs
-0.007 ± 0.07 mmol/l; p < 0.001).
After bariatric surgery we found a significant increase in magnesium levels
(0.84 ± 0.07 mmol/l vs 0.86 ± 0.06 mmol/l;
p = 0.002). In a correlation analysis the
Δ magnesium correlated significantly with
Δ fasting glucose (r = -0.355; p < 0.001),
Δ 1 h glucose (r = -0.201; p = 0.044), Δ 2 h
glucose (r = -0.311; p = 0.002), Δ HbA1c
(r = -0.292; p = 0.001), and Δ bilirubin
(r = 0.197; p = 0.039).
Conclusion: We could show significant
lower magnesium levels in patients with
MO compared with healthy controls.
In addition, we could demonstrate an
increase in magnesium levels, especially
in patients suffering from diabetes after
bariatric surgery.
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Important gender differences
in cardiovascular risk factors in
Austrian patients with morbid
obesity
F. Hoellerl¹, H.-P. Kopp¹, J. M. Brix¹, G. H. Schernthaner2,
S. Kriwanek³, G. Schernthaner¹
1) Department of Internal Medicine I, Rudolfstiftung Hospital Vienna, Vienna, Austria
2) Department of Internal Medicine II, Division of
Austria
3) Department of Surgery, Rudolfstiftung Hospital
Background and aims: The majority of
patients undergoing bariatric surgery are
women. Many studies demonstrated that
women and men have a different risk for
getting cardiovascular (CV) disease. It is
still not clear if morbidly obese men have
the same risk profile as women. Therefore
it was of interest to study a variety of
CV risk factors in a very large group of
Austrian patients with MO (n = 1 015) and
the differences between gender.
Material and methods: We included
1 015 patients with MO (mean age was
40 ± 12 years, 800 females, 215 males). In
the non-DM patients a 75 g oral glucose
tolerance test was performed. Insulin
levels were assessed and HOMA-insu-
Poster 22
Increase in serum magnesium
following weight loss in morbidly
obese patients with type 2 diabetes
J.-M. Brix¹, H.-P. Kopp1, C. Schnack1, S. Kriwanek3,
G. H. Schernthaner², G. Schernthaner1
1) Department of Internal Medicine I, Rudolfstiftung Hospital Vienna, Vienna, Austria
2) Department of Internal Medicine II, Medical
University of Vienna, Vienna, Austria;
3) Department of Surgery, Rudolfstiftung Hospital
Background and aims: Low magnesium
has been associated with insulin resistance
and type 2 diabetes (T2D). In this study
we investigated the magnesium status in
Poster 23
Insulin resistance is associated
with metabolic syndrome but not
with angiographically determined
coronary artery disease
A. Vonbank1,2,3, C. H. Saely1,2,3, P. Rein1,2,3, S.Beer1,2,3,
V. Jankovic1,3, J. Breuss 1,3, C. Boehnel1,3, H. Drexel 1,2,3,4
and Treatment (VIVIT), Feldkirch, Austria
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FID Meeting 2010
2) Department of Medicine and Cardiology,
Background and aims: Insulin resistance
(IR) is the key feature of the metabolic
syndrome (MetS), and in prospective
studies it predicts atherothrombotic
events. However, its association with
directly visualised coronary athero
sclerosis is unclear. We hypothesised that
IR is associated with both angiographi
cally determined coronary artery disease
(CAD) and with the MetS.
Material and methods: We enrolled
986 consecutive patients undergoing
coronary angiography for the evalua
tion of suspected or established stable
CAD; significant CAD was diagnosed
stenoses with lumen narrowing ≥ 50 %. IR
was determined by the HOMA index; the
MetS was defined according to National
Cholesterol Education Programme Adult
Treatment Panel III criteria.
Results: HOMA-IR scores were sig
nificantly higher in MetS patients than
in subjects without the MetS (6.4 ± 2.1
vs 2.2 ± 2.0; p < 0.001). In contrast,
HOMA-IR did not differ significantly
between patients with significant CAD
and those who did not have signifi
cant CAD (4.3 ± 18 vs 3.2 ± 4; p = 0.141).
When both, the presence of the MetS
and of significant CAD, were con
sidered, HOMA-IR was significantly
higher in patients with the MetS both
among those who had significant CAD
(7.2 ± 2.8 vs 2.3 ± 2.1; p < 0.001) and
among those who did not have significant
CAD (5.3 ± 5.7 vs 2.1 ± 1.4; p < 0.001),
whereas it did not differ significantly
between patients with significant CAD
and subjects without significant CAD
in patients with the MetS (7.2 ± 2.8 vs
5.3 ± 5.7; p = 0.679) nor in those without
the MetS (2.1 ± 1.4 vs 2.3 ± 2.1; p = 0.411).
Similar results were obtained when the
IDF definition or the new consensus defi
nition of the metabolic syndrome were
applied.
Conclusion: IR is significantly associated
with the MetS but not with angiographi
cally determined coronary atherosclero
sis.
Poster 24
Insulin resistance, adipokines,
and the expression of metabolic
syndrome in obese individuals with
elevated waist circumference
S. G. Popa1, R. I. Dinu2, M. Mota1, E. Mota3,
C. Stanciulescu4
Diabetes Nutrition and Metabolic Diseases,
Craiova, Romania 2) Clinical County Emergency Hospital, Diabetes
Nutrition and Metabolic Diseases, Craiova,
Romania 3) University of Medicine and Pharmacy Craiova,
Nephrology, Craiova, Romania 4) University of Medicine and Pharmacy Craiova,
Biochemistry, Craiova, Romania
Background and aims: Obesity, especially
abdominal obesity, increases the preva
lence of the metabolic syndrome (MS).
Various adipose tissue factors have been
implicated as biomarkers of the MS. The
aim of this study was to asses which adi
pokines (AK) and insulin resistance (IR)
markers would discriminate the presence
of MS in a strictly obese population with
elevated waist circumference (WC).
Material and methods: The study
included 214 subjects (88 females and
126 males) which had a BMI more
than 25 kg/m2 and had a WC more than
102 cm in males and more than 88 cm
in females. The measured biomark
ers included adiponectin, leptin and
insulin. HOMA-IR was calculated with
the formula: glycaemia (mmol/l) x insulin
(μU/ml)/22.5. MS was defined according
to AHA/NHLBI. Univariate and multi
variate regression analysis were used to
find the associations of variables with MS.
Area under receiver operating character
istic (AUROC) curves analysis was used
to determine the best predictors of MS.
Males with MS had significantly higher
leptin levels (p = 0.001).
Results: Females with MS had significant
ly lower adiponectin levels (p = 0.025) and
higher insulin (p = 0.028) and HOMA-IR
levels (p = 0.028). All measured biomark
ers, except adiponectin, had a statistically
significant correlation to several traits of
the MS, in both sexes, even after adjust
ment for BMI and age.
AUROC curves analysis indicated that
leptin was the single predictor of MS in
males (AUROC = 0,821), and adiponec
tin, insulin and HOMA-IR had statis
tically significant, but poor, diagnostic
value for the detection of MS in females
(AUROC = 0.626, 0.623 and 0.624, respec
tively).
Multiple regression shows that leptin was
the only independent predictor of the MS
status (p = 0.0109) in obese males with
elevated WC included in this study.
Conclusion: In conclusion, in a popula
tion where an excess amount of adipose
tissue exists, leptin is the only reliable
biomarker to discriminate the presence
of MS. We consider that differences in ad
iponectin, insulin and HOMA-IR are a re
flection of their measurements in subjects
with statistically different amounts of
adipose tissue.
Poster 25
Leptin and adiponectin in patients
with venous thromboembolism and
their association with the metabolic
syndrome
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L. Ay1, C. Ay2, C. Bieglmayer3, S. Koder2,
G. Schernthaner1, O. Wagner3, I. Pabinger2
1) Department of Internal Medicine I, Rudolfstiftung
Hospital Vienna, Austria 2) Division of Haematology and Haemostaseology,
Department of Internal Medicine I, Medical University of Vienna, Austria 3) Department of Medical and Chemical Laboratory
Diagnostics, Medical University of Vienna, Austria
Background and aims: The metabolic
syndrome (MetSyn) has been associat
ed with subsequent development of type
2 diabetes and cardiovascular disease.
Recently, the MetSyn has been found to
be also a risk factor for venous thrombo
embolism (VTE). However, the patho
physiological link between the MetSyn
and VTE is yet unknown. Interesting
ly, adipokines, such as adiponectin and
leptin, were reported to be associated
with MetSyn. The aim of the current
study was to investigate whether leptin
and adiponectin are associated with VTE
and MetSyn.
Material and methods: A case-control
study was conducted to investigate the
association of the MetSyn with VTE
in high-risk patients with objective
ly confirmed recurrent VTE, who had
had at least one unprovoked event of
deep venous thrombosis or pulmonary
embolism. Age- and sex-matched healthy
individuals without a history of VTE and
cardiovascular disease served as controls.
FID Meeting 2010
Leptin and adiponetin were measured
by ELISA. A total of 116 patients (53
female/63 male; mean age ± SD: 56 ± 12
years) and 129 controls (66 female/63
male; mean age ± SD: 53 ± 11 years) were
enrolled.
Results: The prevalence of the MetSyn was
statistically significant higher in patients
with VTE (40/116, 35 %) than in controls
(26/129, 20 %, p = 0.012). Serum levels
(median [25. – 75. percentile]) of leptin
and adiponectin did not differ statistically
significant between patients and controls
(15.8 [7.4 – 27.9] vs 12.5 [6.9 – 27.6] ng/
ml; p = 0.36, and 7.8 [6.5 – 10.9] vs 8.2
[5.6 – 10.6] µg/ml; p = 0.54). Patients
with MetSyn had statistically significant
higher leptin levels compared to patients
without the MetSyn (25.3 [15.6 – 36.5]
vs 9.3 [4.6 – 20.0] ng/ml; p < 0.001). Also
controls with MetSyn (n = 26) had statistically significant higher leptin levels
compared to controls without MetSyn
(24.2 [11.9 – 35.6] vs 11.1 [5.6 – 25.7] ng/
ml; p = 0.004). There were no statistically significant differences in adiponectin
levels in patients with MetSyn compared
to those without the MetSyn (7.7 [6.2 – 9.8]
vs 8.2 [6.7 – 11.4] µg/ml; p = 0.16). Controls
with the MetSyn had significantly lower
adiponectin levels compared to those
without the MetSyn (6.4 [5.1 – 7.6] vs 8.8
[6.1 – 11.0] µg/ml; p = 0.002).
Conclusion: In summary, leptin and adiponectin were not associated with VTE.
The presence of the MetSyn was associated with higher leptin serum levels in
the total study population, whereas adiponectin levels were associated with the
presence of MetSyn only in controls.
worldwide. Reduced physical activity (PA)
is considered as largely responsible for
the increasing rate of obesity and obesityrelated diseases. The present study aims
at investigating the relationship between
PA level, body weight and prevalence of
type 2 diabetes (T2DM) among the urban
population of Bulgaria – a country known
to have one of the highest diabetes-related
mortality rates in Europe.
provided information concerning age,
height, body weight, history of T2DM,
arterial hypertension, high cholesterol
levels, cardiovascular disease, self-perception of PA, and motivation for a lifestyle
change. The Baecke PA questionnaire and
the Three Factor Eating Questionnaire
were also completed.
(BMI) 24.7 ± 4.6 kg/m² (mean ± SD). 55 %
had normal body weight, 26 % were overweight, 19 % obese, and 3 % had history
of T2DM. BMI was found to be significantly inversely correlated with sport
and leisure time (p = 0.004; r = -0.220
and p < 0.001; r = -0.295, respectively),
but not with occupational PA. A significantly inverse correlation was observed
between leisure time PA and history of
T2DM, hypertension, and dyslipidaemia
(p = 0.016; r = -0.186, p = 0.038; r = -0.160
and p = 0.027; r = -0.171, respectively).
Sport PA was also inversely correlated
with history of hypertension and dyslipid
aemia (p = 0.011; r = -0.195 and p = 0.05;
r = -0.150, respectively), whereas no correlation between PA at work, T2DM and
any of the other cardiometabolic diseases
was found. In addition, the prevalence
of obesity was found to be significantly higher among subjects in the lowest
when compared to the middle (35.2 %
vs 13.3 %; p = 0.007) and to the highest
tertile of leisure time PA (35.2 % vs 9.6 %;
p = 0.001). Similarly the prevalence of
T2DM was significantly higher in the
lowest, when compared to the middle
(31.5 % vs 14.8 %; p = 0.027) and to the
highest (31.5 % vs 13.2 %; p = 0.02) tertile
of leisure time PA.
Conclusions: A strong inverse relationship was found between the level
of sport and leisure time PA and BMI
and the prevalence of cardiometabolic
disease. The level of PA at work, however,
appeared not to have an effect on body
weight or disease history. Our results are
in accordance with previous findings that
substitution of moderate PA for sedentary
behavior during leisure time already has
a pronounced effect for the prevention
of T2DM.
Poster 27
Metabolic and anti-inflammatory
benefits of eccentric endurance
exercise
P. Rein1,2,3, C. H. Saely1,2,3, A. Vonbank1,2,3,
S. Beer1,2,3, V. Kiene1,2,3, S. Aczel1,2,3, T. Bochdansky1,2,3,
H. Drexel1,2,3,4
Austria
3) Private University of the Principality of Liechtenstein, Triesen, Liechtenstein
4) Drexel University College of Medicine, Philadelphia, PA, USA
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Poster 26
Low physical activity during leisure
time is associated with obesity and
type 2 diabetes among Bulgarian
urban population: Sofia Lifestyle
(SLS) Study
A. Vekova1, T. Stefanov1, I. Bonova2, T. TemelkovaKurktschiev1
1) Medicobiological Unit, International Scientific
2) Unit Sport Pedagogy, International Scientific
Background and aims: The prevalence of obesity is constantly growing,
causing excessive morbidity and mortality
Background and aims: The interplay of
muscle contraction with an external force
can result in one of three types of muscle
activity: shortening or ‘concentric’ when
muscle contraction is stronger than the
external force; lengthening or ‘eccentric’
when the external force is stronger; and
isometric when both forces are equal.
Eccentric endurance exercise (e. g. hiking
downwards) is less strenuous than concentric exercise (e. g. hiking upwards), but
its metabolic effects are largely unknown.
Material and methods: We allocated
93 healthy sedentary individuals to an
exercise intervention program, consisting
of hiking downwards a predefined route
in the Austrian Alps over two months.
For the opposite way, a cable car was used
where compliance was recorded electronically. The difference in altitude was
540 m; the distance was covered three to
five times a week. A matched group of
25 individuals served as a control group.
Fasting and postprandial metabolic
profiles were obtained at baseline and
after the two months period.
Results: Compared with baseline,
eccentric exercise significantly lowered
fasting glucose (97 ± 15 vs 94 ± 9 mg/dl;
p = 0.025) and glucose tolerance (239 ± 50
vs 217 ± 47 mg/dl x h-1; p < 0.001), whereas
both were unchanged in the control
group (p = 0.265 and p = 0.231, respec81
FID Meeting 2010
tively). Body mass index (27.7 ± 4.4 vs
27.4 ± 4.3 kg/m2; p = 0.003) and C-reactive protein (0.27 ± 0.42 vs 0.23 ± 0.25 mg/
dl; p = 0.031) also significantly declined
in the eccentric exercise group, but
not in the control group (p = 0.053 and
p = 0.864, respectively). Furthermore,
eccentric exercise significantly lowered
triglyceride tolerance (1 959 ± 1 330 vs
1 670 ± 1 085 mg/dl x h-1; p = 0.003) and the
postprandial leukocyte count (68.8 ± 11.6
vs 66.5 ± 13.6 G/l x h-1; p = 0.031), whereas
both were unchanged in the control group
(p = 0.819 and p = 0.600, respectively).
Conclusion: Eccentric exercise is a
promising new exercise modality with
favourable metabolic and anti-inflam
matory effects. This moderately strenuous
training option could become especially important in patients with diabetes,
because a large proportion of these
patients suffer from comorbidities conferring a low tolerance for high-intensity
training protocols.
the WHO glucose criteria for diabetes, 13
(12 %) had impaired glucose tolerance
(IGT), 26 (24 %) impaired fasting glucose
(IFG), and 13 (12 %) normal fasting
glucose (NFG). Conversely, the HbA1c
≥ 6.5 % criterion was fulfilled in 58
patients (63 %) with diabetes according
to WHO criteria, in 13 patients (11 %)
with IGT, in 26 patients (8 %) with IFG,
and in 13 patients (2 %) with NFG.
Compared to the standard of WHO
criteria, the proposed HbA1c ≥ 6.5 % for
the diagnosis of diabetes had a sensitivity of 63 % and a positive predictive value
of 53 % for detecting previously undiagnosed diabetes, whereas specificity and
negative predictive value were 95 % and
97 %, respectively.
Conclusions: The recently recommended HbA1c criterion for the diagnosis of
diabetes among CAD patients is highly
specific, but not sensitive. This might
strongly limit its use as a screening tool
for identifying individuals with diabetes.
Poster 28
Poster 29
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New and old criteria for the
diagnosis of diabetes mellitus
in patients with coronary artery
disease
Osteopontin activates human
adipose tissue macrophages
and directly impairs adipocyte
functions
P. Rein1,2,3, C. H. Saely1,2,3, A. Vonbank1,2,3,
C. Boehnel1,3, V. Jankovic1,3, J. Breuss1,3, S. Beer1,2,3,
H. Drexel1,2,3,4
M. Zeyda1, J. Todoric1, O. Aszmann2, G. Prager2,
T. M. Stulnig1
1) VIVIT Institute, Feldkirch, Austria 2) Academic Teaching Hospital Feldkirch,
Feldkirch, Austria 3) Private University of the Principality of Liechtenstein, Triesen, Liechtenstein 4) Drexel University College of Medicine,
Philadelphia, PA, USA
Background and aims: Recently, a
diagnosis of diabetes was recommended with HbA1c ≥ 6.5 %. Data on the concordance of new and old criteria for the
diagnosis of diabetes are very scarce; no
data at all are available for patients with
coronary artery disease (CAD).
Material and methods: We consecutively
enrolled 1 124 Caucasian patients with
angiographically proven CAD who did
not have previously known diabetes. An
oral glucose tolerance test (oGTT) was
performed in all patients.
Results: From the patients with diabetes
according to the new diagnostic criterion
HbA1c ≥ 6.5 % (n = 110), 58 (53 %) fulfilled
82
Materials and methods: Receptor expression was assessed by immunostaining of
human omental adipose tissue sections
and mRNA expression in fractionated
subcutaneous adipose tissue. Human
in vitro differentiated macrophages and
primary adipose tissue macrophages
isolated by flow-cytometry were stimulated with OPN. Human adipocytes, differentiated from primary preadipocytes,
were pretreated or not with OPN prior to
insulin stimulation.
Results: We found broad expression of
OPN receptors in different adipose tissue
cell types including adipocytes. OPN
stimulated phosphorylation of Akt and
MAP kinases, degradation of IκB-α, as
well as secretion of Mcp-1, TNFα, and
IL-10 in model macrophages and isolated
human ATM. Moreover, OPN impaired
differentiation and function of primary
adipocytes as determined by PPARγ and
adiponectin gene expression and insulinstimulated glucose uptake.
Conclusions: OPN activates adipose
tissue macrophages and is able to directly
interfere with adipocyte function. These
results underline the potential use of OPN
as a therapeutic target for obesity-induced
complications.
Acknowledgement: Supported by the
Austrian Science Fund (FWF; Projects
P18776-B11), and the European Community’s 7th Framework Programme
(FP7/2007-2013) under grant agreement
no. 201608 (all to T. M. S).
1) Clinical Division of Endocrinology and
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etabolism, Department of Medicine III, Medical
University Vienna, Vienna, Austria 2) Department of Surgery, Medical University of
Background and aims: Osteopontin
(OPN) is highly upregulated in adipose
tissue in human and murine obesity and
has been recently shown to be functionally involved in the pathogenesis of obesity-induced adipose tissue inflammation
and associated insulin resistance in mice.
OPN is a protein with multiple functions
and acts as a chemokine and an inflammatory cytokine through a variety of
different receptors (CD44, integrins). It
is expressed in many cell types including
adipose tissue macrophages (ATM).
However, the target cells of OPN action
in obese adipose tissue are still elusive.
Hence, we aimed to investigate expression of OPN receptors and the impact of
OPN on ATM, adipocytes and other cells
of human adipose tissue.
Poster 30
Prediction of type 2 diabetes in
angiographied coronary patients
with the novel metabolic syndrome
consensus definition: the importance
of waist circumference
C. H. Saely 1,2,3, A. Vonbank 1,2,3, P. Rein 1,2,3, S. Beer 1,2,3,
T. Gansch 1,2,3, S. Greber1,2,3 H. Drexel 1,2,3,4
Background and aims: Recently,
important international societies,
FID Meeting 2010
including IDF, NHLBI, and AHA, have
put forth a novel consensus definition of
the metabolic syndrome (MetS) in order
to harmonize its use in clinical practice.
This new MetS definition allows both the
IDF and the NCEP-ATP III cutoffs for the
diagnosis of a large waist in Caucasians.
Its power to predict the incidence of type
2 diabetes (T2DM) is unknown.
Material and methods: We prospectively
recorded the incidence of T2DM over 8
years in a population of 506 consecutive
non-diabetic Caucasian patients undergoing coronary angiography for the evaluation of stable coronary artery disease.
Results: At baseline, 49.8 % (n = 252)
of our patients had the MetS according
to the novel criteria, when the lower
IDF waist cutoffs (≥ 94 cm in men and
≥ 80 cm in women) were used, and
39.7 % (n = 201), when the NCEP-ATPIII waist cutoffs (≥ 102 cm in men and
≥ 88 cm in women) were applied. During
the follow-up period, T2DM was newly
diagnosed in 107 patients; the incidence
rates of T2DM significantly increased
from subjects without the MetS over the
intermediate group, who had the MetS
with the lower IDF waist cutoffs, to
patients, who had the MetS, also when
the more selective NCEP- ATP-III waist
cutoff values were aplied (13.8 %; 15.7 %;
31.8 %; p trend < 0.001). Even after multivariable adjustment, T2DM risk was significantly higher in patients with a MetS
diagnosis, based on the more selective
NCEP-ATPIII waist cutoffs, than in the
intermediate group (odds ratio 2.54
[1.12 – 5.73]; p = 0.025).
Conclusions: We conclude that the 8-year
incidence of diabetes in non-diabetic
patients undergoing coronary angiography who meet the novel MetS criteria
is very high, especially when the more
selective NCEP ATP-III waist circumference cutoff values are applied.
Background and aims: Obesity, particularly abdominal obesity, represents one of
the cardiovascular risk factors. Available
data suggest that the prevalence is more
than twice as high at age 55 as at age 20
and women are more affected than men.
The objective of our study was to investigate the prevalence of obesity in
patients with type 2 diabetes mellitus and
euthyroid diffuse goiter, and the association with other cardiovascular risk factors.
Materials and methods: We investigate
125 patients with type 2 diabetes mellitus
and euthyroid diffuse goiter (111 female
and 14 male). We evaluated the lipid
profile (total cholesterol, triglycerides,
HDL cholesterol, LDL cholesterol), the
systolic and diastolic blood pressure,
fasting glycaemia and the abdominal circumference and body mass index (BMI).
Results: 72 % of subjects had a BMI
> 30 kg/m2 (90 % F and 10 % M, p < 0.001,
χ2 = 115.2) and 22.4 % a BMI between 25
and 29,9 kg/m2 (85.71 % F and 14.28 % M,
p < 0.001, χ2 = 28.57).
As to the degree of obesity: 40.67 % had
obesity grade I (89.58 % F and 10.41 % M,
p < 0.001, χ2 = 60.17), 22.03 % obesity grade
II (84.61 % F and 15.38 % M, p < 0.001,
χ2 = 24.92m and 13.55 % obesity grade III
(100 % F and 0 % M, p < 0.001, χ2 = 32).
From obese and overweight subjects
57.62 % showed elevated concentrations of total cholesterol, 10.16 % showed
elevated concentrations of triglycerides,
and 68.64 % had hypertension.
Conclusions: In patients with type 2
diabetes mellitus and euthyroid diffuse
goiter, a predominance of obesity in female
exists. Concerning the degree of obesity,
the obesity grade I prevails. Because of
the association with other cardiovascular
risk factors, early detection of obesity is
important in this subjects’ group.
P o s t e r 31
Risk scores in the prediction of
incident type 2 diabetes: MONICA/
KORA Augsburg case-cohort study
Background and aims: Systemic concentrations of acute-phase proteins,
cytokines, chemokines and soluble
adhesion molecules are associated with
the risk of type 2 diabetes. The association
of each of these biomarkers alone with
incident diabetes is too weak for the prediction of the disease, but the predictive
value of combinations of multiple inflammation-related biomarkers is still unclear.
This study aims to address the following
questions: (i) What is the predictive value
of inflammation-related biomarkers for
incident type 2 diabetes? (ii) Are these
predictive values comparable with those
of established biomarkers of cardiometabolic risk? (iii) Can the predictive value
be improved by combining both sets of
risk factors?
Materials and methods: The study investigated inflammation-related biomarkers (measured in non-fasting
serum samples) and additional cardiometabolic risk factors in a prospective
case-cohort study within the population-based MONICA/KORA Augsburg
cohort. Analyses are based on 436 individuals with and 1 413 individuals
without incident type 2 diabetes. The
follow-up was 10 ± 5 years. Receiver
operator characteristic (ROC) analyses
were used to calculate areas under the
ROC curve (AROC) for different sets of
risk factors: (a) basic model: adjusted for
age, sex, and survey; (b): immunological
model: factors from (a) plus CRP, IL-6,
IL-18, MIF, TGFβ1, MCP-1, IL-8, IP-10,
RANTES, adiponectin, leptin, sE-selectin, sICAM-1; (c) cardiometabolic model:
factors from (a) plus BMI, systolic blood
pressure, total cholesterol/HDL cholesterol ratio, parental history of diabetes or
myocardial infarction (according to the
respective endpoint), smoking, alcohol,
physical activity; (d) full model: combination of risk factors in (b) and (c).
Results: For the prediction of type 2
diabetes, the AROC for the basic model
was 0.733. Addition of either inflammation-related biomarkers (as continuous variables; model b) or cardiometabolic risk factors (model c) resulted in
an increase to 0.803 in both models.
Addition of adiponectin and sE-selectin
to model c led to the most pronounced
increase in AROC (0.827 and 0.824, respectively) among all immune mediators.
A combination of all risk factors predicted
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Prevalence of obesity and association with other cardiovascular
risk factors in patients with type
2 diabetes mellitus and euthyroid
diffuse goiter
A. Gherbon1, L. Noveanu1, G. Mihalas1
1) Department of Physiology – UMF ’V. Babeş‘
Timişoara, Romania
Poster 32
C. Herder1, J. Baumert2, A. Zierer2, M. Roden1,
C. Meisinger2, W. Koenig3, B. Thorand3
1) German Diabetes Center, Duesseldorf,
Germany
2) Helmholtz Zentrum Muenchen, Neuherberg,
Germany
3) University of Ulm Medical Center, Ulm,
Germany
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FID Meeting 2010
type 2 diabetes with an AROC of 0.845.
Conclusions: The addition of multiple
inflammation-related biomarkers to a
basic prediction model and to a model
including cardiometabolic risk factors
increased the AROC in the prediction of
type 2 diabetes.
Poster 33
Significant association of TCF7L2
variant rs7903146 with angiographically characterized coronary
artery disease in women
A. Muendlein1,2,3, C. H. Saely1,2,3, S. Geller-Rhomberg1,2,3, G. Sonderegger1,2,3, P. Rein1,2,3, T. Winder1,2,3,
S. Beer1,2,3, A. Vonbank1,2,3, H. Drexel1,2,3,4
Austria 3) Private University of the Principality of Liechtenstein, Triesen, Liechtenstein 4) Drexel University College of Medicine,
justment for age, smoking, BMI, total
and HDL cholesterol did not significantly change this finding (OR = 1.37
[1.06 – 1.78]; p = 0.016). Also, after further
adjustment for T2DM, the association
between rs7903146 and CAD remained
significant (OR = 1.31 [1.00 – 1.70];
p = 0.047). Further, the extent of CAD
significantly increased from subjects
who were homozygous for the C allele
over heterozygous subjects to those who
carried the TT genotype (0.79 ± 1.45 vs
0.95 ± 1.40 and 0.98 ± 1.50, respectively;
p = 0.022). Similarly, a significant association between SNP rs7903146 and the
severity of coronary lesions was observed
(severity scores of 26.1 ± 36.7, 35.7 ± 39.9,
and 36.7 ± 39.4 for the CC, CT, and TT
genotype, respectively; p = 0.004).
Conclusion: We conclude that TCF7L2
variant rs7903146 is significantly associated with angiographically diagnosed
CAD in women.
(42.5 % vs 51.0 %; p = 0.010). The prevalence rates of significant CAD in patients
with the MetS vs individuals without MetS
were 69.2 % vs 62.6 %; p = 0.080 in men
and 44.8 % vs 32.2 %; p = 0.015 in women.
Serum concentrations of CRP were significantly higher in patients with the MetS
compared to subjects without the MetS
both in men (0.47 ± 0.68 vs 0.36 ± 0.51 mg/
dl; p < 0.001) and in women (0.44 ± 0.52 vs
0.33 ± 0.44 mg/dl; p = 0.005). In contrast,
CRP did not differ significantly between
patients with significant CAD and those
who did not have significant CAD in
either gender (p = 0.105 for women and
p = 0.461 for men). When all MetS traits
were entered simultaneously into one
ANCOVA model, in men only the low
HDL-C criterion proved to be independently associated with CRP (F = 36.65;
p < 0.001), whereas in women the low
HDL-C and the high glucose criteria significantly predicted serum CRP after multivariable adjustment (F = 5.55; p = 0.019
and F = 5.31; p = 0.022, respectively).
Conclusion: CRP is strongly associated
with the MetS, but not with angiographically diagnosed coronary atherosclerosis
in men and women. The overall association of the MetS with subclinical inflammation both in men and women is driven
by the low HDL cholesterol feature and in
women additionally by the high glucose
feature.
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Background and aims: Type 2 diabetes
mellitus (T2DM) confers a particularly high risk of coronary artery disease
(CAD) in women. Variations in the
transcription factor 7-like 2 (TCF7L2)
gene, particularly rs7903146, increase
T2DM risk; their association with CAD
is uncertain. In particular, potential links
between TCF7L2 variant rs7903146 and
CAD in women are unknown.
Material and methods: We therefore
investigated the association between
rs7903146 and angiographically determined CAD in a cohort of 554 female
Caucasian patients undergoing coronary
angiography for the evaluation of established or suspected CAD. At angiography, significant CAD was diagnosed
stenoses with lumen narrowing of ≥ 50 %.
The severity of CAD was calculated as
the sum of all stenosis percentages of a
given patient divided by the number of
coronary stenoses in this patient and
the extent as the number of significant coronary stenoses. The association between rs7903146 and CAD was
evaluated in an additive genetic model.
Results: Variant rs7903146 was significantly associated with angiographically
characterized CAD (additive odds ratio
(OR) = 1.37 [1.07 – 1.76]; p = 0.011). Ad84
Poster 34
Subclinical inflammation, the
metabolic syndrome, and coronary
atherosclerosis in men and women
S. Beer1,2,3, P. Rein1,2,3, C. H. Saely1,2,3, A. Vonbank1,2,3,
C. Boehnel1,3, V. Jankovic1,3, J. Breuss1,3,
A. Muendlein1,2,3, H. Drexel1,2,3,4
Austria 3) Private University of the Principality of Liechtenstein, Triesen, Liechtenstein 4) Drexel University College of Medicine,
Background and aims: The metabolic
syndrome (MetS) and stable coronary
artery disease (CAD) frequently coincide;
the individual contributions of these
entities to subclinical inflammation are
unknown.
Material and methods: We enrolled 1 012
consecutive patients, 656 men and 356
women, undergoing coronary angiography for the evaluation of suspected or
established stable CAD. The MetS was
defined according to the AHA revision
of the NCEP ATP-III criteria; coronary
stenoses with lumen narrowing ≥ 50 %
were considered to be significant.
Results: The proportion of patients with
the MetS was lower in men than in women
Poster 35
The soluble form of the receptor of
advanced glycation endproducts
(sRAGE) increases after bariatric
surgery in morbid obesity
J. M. Brix¹, F. Hoellerl¹, H.-P. Kopp1,
G. H. Schernthaner2, G. Schernthaner¹
1) Department of Internal Medicine I, Rudolfstiftung Hospital Vienna, Vienna, Austria 2) Department of Internal Medicine II, Division of
Austria
Background and aims: The increased cardiovascular disease (CVD) risk in patients
with morbid obesity (MO) cannot be
fully explained by traditional CV risk
factors. Recent studies have shown that
low levels of sRAGE are associated with
an increased risk for CVD. Activation of
the receptor of advanced glycation endproducts (RAGE) leads to inflammation
FID Meeting 2010
via the NFκB pathway. sRAGE can bind
to RAGE and avoids the interaction of
RAGE with proinflammatory ligands.
Therefore we investigated sRAGE levels
in patients with MO compared to healthy
lean controls (CO), as well as before and
after bariatric surgery (BS).
Materials and methods: We included 85
patients (mean age: 41 ± 12 years; mean
BMI: 45.4 ± 7.9 kg/m²) with MO in comparison with 40 CO (mean age: 42 ± 13
years; mean BMI: 26.0 ± 5.5 kg/m²). All
patients were investigated before and 2
years after BS. Apart from weight and CV
risk-markers (blood pressure, lipids), a
glucose tolerance test (75 g), renal and
inflammation parameters were assessed.
sRAGE levels were assessed by a commercial ELISA.
Results: Patients with MO had significantly lower sRAGE levels than CO:
1 010 ± 514 pg/ml vs 1 501 ± 674 pg/
ml; p < 0.001. In the longitudinal study,
sRAGE levels increased significantly after
BS: 1 010 ± 514 pg/ml vs 1 261 ± 710 pg/
ml; p = 0.008. In the correlation analysis
Δ sRAGE levels were associated with
Δ 1 hour postprandial glucose (R = 0.35;
p = 0.037), Δ 2 hour postprandial glucose
(R = -0.38; p = 0.024), Δ fasting insulin
(R = -0.59; p < 0.001), Δ 2 hour post
prandial insulin (R = -0.76; p < 0.001),
Δ HOMA-insulin resistance (IR = -0.60;
p < 0.001), Δ γ-glutamyl transferase
(R = -0.36; p = 0.014) and Δ triglycerides
(R = -0.30; p = 0.034). In a multivariate
model, Δ 1 hour postprandial glucose
(β = 0.227; p = 0.027), Δ 2 hour post
prandial glucose (β = 0.303; p = 0.027),
Δ 2 hour postprandial insulin (β = -0.597;
p = 0.005) and Δ HOMA-IR (β = -0.418;
p = 0.019) predicted Δ sRAGE.
Conclusion: Patients with MO have significantly lower sRAGE levels compared
with CO, but sRAGE levels increase significantly after BS. Since high sRAGE
levels inhibit the activation of inflam
matory pathways, our results might help
to understand the beneficial effects of
bariatric surgery regarding CV morbidity
and mortality.
cohort study on angiographically
characterized coronary patients
C. H. Saely1,2,3, P. Rein1,2,3, A. Vonbank1,2,3, T. Gansch1,
S. Greber1, C. Boehnel1,3, V.Jankovic1,3, H. Drexel1,2,3,4
C. H. Saely1,2,3, T. Gansch1, A. Vonbank1,2,3, P. Rein1,2,3,
S. Beer1,2,3, S. Greber1, H. Drexel1,2,3,4
Austria
4) Drexel University College of Medicine,
1) VIVIT Institute, Feldkirch, Austria
2) Academic Teaching Hospital Feldkirch,
Feldkirch, Austria
4) Drexel University College of Medicine,
Background and aims: Current guidelines
consider diabetes as a coronary artery
disease (CAD) risk equivalent, but cardiovascular risk in patients with diabetes
may vary substantially depending on the
presence of subclinical CAD at baseline.
Material and methods: Vascular events
were recorded over 8 years in 750 consecutive patients undergoing coronary
angiography for the evaluation of established or suspected stable CAD.
Results: From our patients, 244 had
neither type 2 diabetes (T2DM) nor significant CAD (i. e. coronary stenoses
≥ 50 %) at the baseline angiography, 50
had T2DM but not significant CAD, 342
did not have T2DM but had significant
CAD, and 114 had both T2DM and significant CAD. Non-diabetic subjects
without significant CAD had an event rate
of 20.5 %. The event rate was similar in
T2DM patients without significant CAD
(22.0 %; p = 0.811), but higher in nondiabetic patients with significant CAD
(39.5 %, p < 0.001). Patients with T2DM
plus significant CAD had the highest
event rate (53.5 %; p < 0.001). Importantly,
T2DM patients without significant CAD
had a significantly lower event rate than
non-diabetic patients with significant
CAD (p = 0.017).
Conclusions: T2DM per se is not a CAD
risk equivalent. Moderate risk diabetic
patients without significant CAD and
very high-risk diabetic patients with significant CAD add up to a grand total of
high risk diabetic patients: this is why
diabetes appears as a CAD risk equivalent in many epidemiological studies.
Background and aims: We aimed at prospectively investigating the impact of the
left ventricular ejection fraction (LVEF)
and of angiographically verified coronary
artery disease (CAD) on the risk of cardiovascular events in patients with type
2 diabetes (T2DM) and in non-diabetic
subjects.
Material and methods: Cardiovascular
events were recorded over 8 years in 629
consecutive patients undergoing coronary
angiography for the evaluation of established or suspected stable CAD. At the
baseline angiography, significant CAD
was diagnosed in the presence of significant coronary stenoses with lumen
narrowing ≥ 50 %, and the baseline LVEF
was determined invasively by ventriculography.
Results: The baseline prevalence of significant CAD was higher (68.6 % vs 55.5 %;
p = 0.006) in patients with T2DM (n = 137)
than in non-diabetic subjects (n = 492);
the baseline LVEF was similar in these two
patient subgroups (65 ± 15 % vs 67 ± 15 %;
p = 0.253). Prospectively, significant
CAD (HR = 2.07 [1.50 – 2.88]; p < 0.001)
and the LVEF (standardised HR = 0.79
[0.71 – 0.88]; p < 0.001) after multivariable adjustment both proved to be significantly predictive of cardiovascular events
in a mutually independent manner. The
incidence of vascular events was significantly higher in patients with T2DM than
in non-diabetic subjects (43.8 % vs 30.1 %;
p = 0.003). In analyses with respect to the
diabetes status, the LVEF strongly and
significantly predicted cardiovascular
events in non-diabetic subjects (HR = 0.72
[0.62 – 0.82]; p < 0.001) but not in patients
with T2DM (1.00 [0.75 – 1.22]; p = 0.711).
An interaction term LVEF*T2DM was
significant (p = 0.047), indicating that the
cardiovascular risk conferred by a low
LVEF was significantly higher in non-diabetic subjects than in patients with T2DM.
The presence of significant CAD proved to
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Poster 36
Type 2 diabetes is not a coronary
heart disease risk equivalent:
results from an 8-year prospective
Poster 37
Type 2 diabetes significantly
modulates the impact of low left
ventricular ejection fraction on the
risk of cardiovascular events
85
FID Meeting 2010
be significantly and independently predic
tive of vascular events both in non-dia
betic subjects and in patients with T2DM
(HR = 1.84 [1.26 – 2.67]; p = 0.001 and 2.45
[1.18 – 5.06]; p = 0.016, respectively).
Conclusion: From the results of this 8-year
prospective cohort study we conclude that
T2DM significantly modulates the car
diovascular risk conferred by a low left
ventricular ejection fraction.
Poster 38
Type 2 diabetes and the risk of
colorectal cancer – a retrospective
10-year study
V. Negrean1, M. Cazacu2, T. Alexescu1, M. Adam1,
A. Tantau1
1) Medicala 4 Clinic, University of Medicine and
Pharmacy ‘Iuliu Hatieganu’ 2) Chirurgie 4 Clinic, University of Medicine and
Pharmacy ‘Iuliu Hatieganu’
1 parent in 10 (15.64 %), for 2 parents
(mother and father) in 7 cases (8.82 %),
other relatives with T2DM in 16 cases
(24.46 %), and positive family history
(parents) was found in our collective in
8 (12.32 %) subjects for colorectal cancer,
and 14 (21.56 %) for other malignancies.
We found a late diagnosis of type 2 diabetes
and colorectal cancer (in 4th stage) in 12
(18.48 %) subjects, peritoneal carcinoma
tosis was present in 13 (23.10 %) subjects,
totalizing 25 cases (41.58 %) of patients
with disseminated disease.
Regarding the treatment, most of our
subjects (14; 21.56 %) received bigu
anides, followed by sulfonylureas (12;
18.48 %).
Conclusions: Type 2 diabetes represents
a risk factor for colon cancer, especially
in subjects with increased BMI, a possible
cause could be the insulin resistance.
compared to group I (p < 0.05) in at least
one of the three vascular regions (arteries
of the lower extremities, carotid arteries,
coronary arteries). The greatest difference
was seen in coronary events.
Conclusions: Hence raised Lp(a) is an
important, independant cardiovascular
risk factor. We conclude that Lp(a) should
therefore be determined in all patients
with increased atherogenic risk. Nicotinic
acids are the only drugs that can lower
Lp(a). In patients with raised levels of
Lp(a) optimal management of cardiac risk
factors is essential, with a LDL-cholesterol
goal of < 2.6 or < 1.8 mmol/l.
Poster 40
Effect of fenofibrate on the level
of asymmetric dimethylarginine in
patients with diabetes mellitus
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Background and aims: Diabetes mellitus
is a disease with increasing prevalence,
similar to the colon cancer. Some authors
showed the existence of a link between
type 2 diabetes and colorectal cancer. The
purpose of the study is to evaluate type
2 diabetes as a risk factor in colorectal
cancer.
Material and methods: We studied a
number of 65 patients with type 2 diabetes
and colorectal cancer all diagnosed and
treated in CF Hospital of Cluj Napoca
during a period of 10 years. Parameters
assessed were: BMI, abdominal circumfer
ence, the period of time elapsed between
the onset of diabetes, the moment of ap
parition of the first digestive symptom,
prescribed therapy, blood group, family
history.
Results: 27 patients (41.58 %) of the 65
patients were women and 35 (58.42 %)
were men. There were 76.90 % (50
patients) from urban areas and there were
15 patients (23.10 %) from rural areas.
A2 blood group was found in 50 patients
(76.40 %). Regarding the BMI, 86.14 %
of the patients were obese, and the age at
which colorectal cancer was diagnosed
was above 50 years (91.30 %); history of
the metabolic disease below 5 years was
present in 49,28 % and more than 10 years
in 12,32 %. We mention that 4 patients
(6.16 %) had simultaneously the diagnosis
of type 2 diabetes and colorectal cancer.
Positive family history for diabetes: for
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Poster 39
Raised lipoprotein (a) levels
are an important predictor for
cardiovascular events
U. Schatz1
1) University Clinic Carl Gustav Carus, Dresden,
Germany.
Background and aims: There is growing
evidence of lipoprotein (a) (Lp(a)) as a
risk factor for cardiovascular disease.
In this study, we investigated the corre
lation between the level of Lp(a) and the
incidence of cardiovascular events.
Material and methods: Patients of our
lipid outpatient clinics were devided into
3 groups depending on the level of Lp(a):
Group I: Lp(a) 807 – 1 129 mg/l, Group II:
Lp (a) 1 131 – 1 461 mg/l, Group III: Lp (a)
1 470 – 3 697 mg/l. 168 patients (93 male,
75 female) were included.
Results: 35 % of all patients with raised
Lp(a) levels (800 mg/l) had cardiovascu
lar events.
Regarding other cardiovascular risk
factors such as BMI, dyslipoproteinaemia,
diabetes, hypertension, family history for
CVD, age and sex, there was no signifi
cant difference between the three groups
(χ2-test).
The three groups differed in the occurence
of cardiovascular events (χ2-test, p<0.05).
A 2.5-fold higher risk for cardiovascu
lar events was observed in group III
P. Dunev1, L.Vladimirova-Kitova1, F. Nikolov1
1) Clinic of Cardiology, Medical University, Plovdiv,
Bulgaria
Background and aims: Clinical studies
have demonstrated that long-term
treatment with fenofibrate can hinder the
progress of atherosclerosis. It has been
reported that fenofibrate attenuates ox
idative-LDL-induced impairment of en
dothelium-dependent vasodilation in hy
perlipidaemic patients. The recent study
has shown that fenofibrate attenuated
endothelial dysfunction via reduction of
ADMA production in diabetes mellitus
patients. This study wants to test whether
treatment with fenofibrate decreases
asymmetric dimethylarginine (ADMA)
and total homocysteine level in diabetes
mellitus.
Material and methods: In the present
study, 60 subjects with diabetes mellitus
were recruited to receive treatment with
micronized fenofibrate (160 mg/d).
Serum concentrations of ADMA, total
homocysteine and flow-mediated va
sodilation were measured. Endotheli
al function assessed by flow-mediated
dilation (FMD) of the brachial artery
was performed.
Results: Compared with control, serum
levels of ADMA (0.58 ± 0.04 μmol/l in
control and 0.60 ± 0.33 μmol/l in diabetic
patients, p < 0.01), 17.5 ± 3.5 μmol/l -ho
mocysteine were markedly elevated,
concomitantly with impaired endo
FID Meeting 2010
thelium-dependent vasodilation in individuals with hypertriglyceridaemia (4.5 ± 2.1 %). 2-months treatment
with fenofibrate significantly reduced
the elevated levels of ADMA (after
treatment 0.53 ± 0.12 μmol/l, p < 0.01),
total homocysteine (after treatment
10.5 ± 3.0 μmol/l), and improved the endothelial function (8.5 ± 1.5 %).
Conclusions: These results suggest that
the beneficial effect of fenofibrate on the
endothelium in diabetic individuals may
be related to reduction of ADMA and
total homocysteine levels.
Poster 41
diabetes mellitus and 30 controls. The
middle age of the subjects was 50 ± 5;
sex m/f(DM patients) 35/15 ; sex m/f
(controls) 14/16. Serum concentrations
of ADMA levels were measured with
ELISA method.
Results: Compared with control, serum
levels of ADMA (0.52 ± 0.5 μmol/l in
control and 1.54 ± 0.5 μmol in diabetes
mellitus patients, P < 0.001) were
markedly elevated in subjects with DM.
Conclusions: These results suggest that
the elevated ADMA in diabetes could
contribute to endothelial dysfunction
and accelerated atherosclerosis in this
population.
Plasma levels of the asymmetric
dimethylarginine in patients with
diabetes mellitus
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P. Dunev1, L.Vladimirova-Kitova1, F. Nikolov1
1) Clinic of Cardiology, Medical University, Plovdiv,
Bulgaria
Background and aims: Cardiovascular complications are the major cause
of mortality and morbidity for the 135
million individuals worldwide afflicted
by type 2 diabetes mellitus (DM). Endothelial dysfunction is a common feature
in diabetic patients and may contribute
to cardiovascular morbidity. Nitric oxide
(NO) is a well-recognized anti-atherogenic factor; it inhibits the inflammatoryproliferative processes in atherosclerosis.
Indeed, endothelial dysfunction due to
reduced synthesis and/or bioavailability
of NO is thought to be an early step in the
course of atherosclerotic cardiovascular
disease (CVD). NO is synthesized from
L-arginine via the action of NO synthase
(NOS), which is known to be blocked by
endogenous L-arginine analogues such as
asymmetric dimethylarginine (ADMA),
a naturally occurring amino acid found
in plasma and various types of tissues.
Asymmetric dimethylarginine (ADMA)
has evolved as an important regulator
of nitric oxide (NO) synthesis in recent
years. Elevated levels of ADMA have been
reported in many conditions associated
with a high cardiovascular risk.This study
aims on demonstrating that plasma levels
of ADMA are elevated in patients with
diabetes.
Material and methods: In the present
study we recruited 50 subjects with
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Diabet, Nutriţie, Risc Cardiometabolic

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