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Vienna, Austria

Aumueller E.,University of Vienna | Remely M.,University of Vienna | Baeck H.,University of Vienna | Hippe B.,University of Vienna | And 2 more authors.
Journal of Nutrigenetics and Nutrigenomics | Year: 2015

Background/Aims: Diabetes mellitus type 2 (DMT2) is accompanied by systemic low-grade inflammation with elevated levels of interleukin-6 (IL-6), which is encoded by a gene (IL-6) previously shown to be regulated by DNA methylation. We investigated seven CpG sites in IL-6 in individuals with DMT2, obese individuals and lean controls. Further, the DMT2 group received the glucagon-like peptide 1 agonist liraglutide. Methods: Blood samples were taken at the beginning of the study and after 4 months. The DNA methylation was assessed using pyrosequencing. Results: Methylation levels at the CpG sites -664, -628 and +13 at the first sampling time point (T1) and at -666 and -664 at the second sampling time point (T2) correlated negatively with initial body weight in the DMT2 group. We found positive correlations for the obese and the lean control group. In the obese group, CpG +27 methylation at T1 correlated with initial body weight (r = 0.685; p = 0.014). In the lean group, CpG -664 at T1 (r = 0.874; p = 0.005) and CpG -628 at T2 (r = 0.632; p = 0.050) correlated with initial body weight. Conclusion: These findings are an informative basis for further studies to elucidate epigenetic mechanisms underlying DMT2. Additionally, our results might provide starting points for the development of biomarkers for prevention and therapy strategies. © 2015 S. Karger AG, Basel. Source


Stadler M.,Hietzing Hospital | Stadler M.,Karl Landsteiner Institute of Metabolic Diseases and Nephrology | Stadler M.,Kings College London | Tomann L.,Karl Landsteiner Institute of Metabolic Diseases and Nephrology | And 11 more authors.
European Journal of Endocrinology | Year: 2014

Abstract Objective: To stop smoking is commonly associated with significant weight gain, but the mechanisms for this are poorly understood. We assessed the effects of smoking cessation on body weight, insulin sensitivity, b-cell function, and appetite. Subjects and methods: Twenty-seven long-term smokers (nZ27; nine females/18 males, 28G1 years, 22.9G0.6 kg/m2) attending an ambulatory smoking cessation program in a community hospital in Vienna, Austria were examined at baseline (Visit A; still smoking) and after a minimum of 3 months of smoking abstinence (Visit B; nZ14); relapsed smokers were not followed up. Participants underwent 3-h oral glucose tolerance tests and body composition measurements at each study visit. Fasting (QUICKI) and dynamic (oral glucose insulin sensitivity (OGIS)) insulin sensitivity and b-cell secretion (insulinogenic index 140 (IGI40)) were calculated. Food intake was quantified with a free choice buffet. Fasting plasma concentrations of neuropeptide-Y (NPY), peptide-YY (PYY), glucagon-like peptide 1 (GLP1), leptin, ghrelin, and visfatin were measured. Results: After O3 months' smoking abstinence, body weight, and fat mass were increased (C4 and C22% respectively, P!0.05) and fasting insulin sensitivity deteriorated (QUICKI: post, 0.37G0.02 vs baseline, 0.41G0.2; P!0.05), while OGIS remained unchanged throughout. IGI40 increased by 31% after O3 months' smoking abstinence (P!0.01). Carbohydrate ingestion increased after stopping smoking (P!0.05). NPY fasting levels were increased after O3 months (P!0.05), PYY, GLP1, leptin, ghrelin, and visfatin were unchanged. Conclusion: Smoking cessation is associated with transient metabolic changes including increased b-cell secretion in response to glucose and fasting insulin resistance. These alterations may be associated with or contribute to the body weight gain after smoking cessation. © 2014 European Society of Endocrinology Printed in Great Britain. Source

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