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CLINICAL STUDIES |
1 Department of Sport Medicine, Third Faculty of Medicine, Charles University in Prague, 100 00 Prague, Czech Republic2 Division of Cell and Molecular Biology, Third Faculty of Medicine, Center of Biomedical Sciences, Charles University in Prague, 100 00 Prague, Czech Republic3 Institute of Preventive Medicine, Copenhagen University Hospital, DK-1357 Copenhagen, Denmark4 Department of Human Nutrition, Faculty of Life Sciences, University of Copenhagen, DK-1958 Copenhagen, Denmark5 Department of Human Biology, Nutrition and Toxicology Research Institute, Maastricht University, 6200 MD Maastricht, The Netherlands6 School of Biomedical Sciences, Queen's Medical Centre, University of Nottingham Medical School, Nottingham, NG7 2UH UK7 Department of Nutrition, Hotel-Dieu Hospital, University Pierre-et-Marie Curie, F-75006 Paris, France8 Obesity Research Unit, INSERM U586, Louis Bugnard Institute and Clinical Investigation Centre, Toulouse University Hospitals, Paul Sabatier University, F-31432 Toulouse, France9 Department of Physiology and Nutrition, University of Navarra, ES-31008 Pamplona, Spain10 Franco-Czech Laboratory for a Clinical Research on Obesity, Charles University and INSERM, 100 00 Prague, Czech Republic
(Correspondence should be addressed to J Polak who is now at 3 Lekarska Fakulta University Karlovy, Ustav Telovychovneho Lekarstvi CPL, Ruska 87, Prague 10, 100 00, Czech Republic; Email: jan.polak{at}lf3.cuni.cz)
Aim: Adiponectin increases insulin sensitivity, protects arterial walls against atherosclerosis, and regulates glucose metabolism, and is decreased in obese, insulin resistant, and type 2 diabetic patients. Adiponectin circulates in plasma as high, medium, and low molecular weight forms (HMW, MMW, and LMW). The HMW form was suggested to be closely associated with insulin sensitivity. This study investigated whether diet-induced changes in insulin sensitivity were associated with changes in adiponectin multimeric complexes.
Subjects: Twenty obese women with highest and twenty obese women with lowest diet induced changes in insulin sensitivity (responders and non-responders respectively), matched for weight loss (body mass index (BMI)=34.5 (S.D. 2.9) resp. 36.5 kg/m2 (S.D. 4.0) for responders and non-responders), were selected from 292 women who underwent a 10-week low-caloric diet (LCD; 600 kcal/d less than energy requirements). Plasma HMW, MMW, and LMW forms of adiponectin were quantified using Western blot method.
Results: LCD induced comparable weight reduction in responders and non-responders by 8.2 and 7.6 kg. Homeostasis model assessment insulin resistance index decreased by 48.1% in responders and remained unchanged in non-responders. Total plasma adiponectin and the quantity of HMW and MMW remained unchanged in both groups, while LMW increased by 16.3% in non-responders. No differences between both groups were observed at baseline and after the study. Total plasma adiponectin, MMW, and LMW were negatively associated with fasting insulin levels at baseline.
Conclusion: No differences in total plasma adiponectin, HMW, MMW, and LMW forms were observed between responders and non-responders following 10-week LCD, suggesting that adiponectin is not a major determinant of weight loss-induced improvements in insulin sensitivity.
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