Postprandial Adiponectin Levels Are Unlikely to Contribute to the Pathogenesis of Obesity in Prader-Willi Syndrome

Aim:To investigate fasting and postprandial adiponectin levels in PWS patients as compared to obese and lean subjects and whether they could contribute to the pathogenesis of obesity in this syndrome. Methods: We studied 7 patients with PWS, 16 obese patients and 42 lean subjects for the fasting stu...

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Veröffentlicht in:Hormone research 2006-01, Vol.65 (1), p.39-45
Hauptverfasser: Caixàs, Assumpta, Giménez-Palop, Olga, Giménez-Pérez, Gabriel, Potau, Neus, Berlanga, Eugenio, González-Glemente, José-Miguel, Arroyo, Jaume, Laferrère, Blandine, Mauricio, Dídac
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Sprache:eng
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Zusammenfassung:Aim:To investigate fasting and postprandial adiponectin levels in PWS patients as compared to obese and lean subjects and whether they could contribute to the pathogenesis of obesity in this syndrome. Methods: We studied 7 patients with PWS, 16 obese patients and 42 lean subjects for the fasting study. From this group, we evaluated 7 patients with PWS, 7 age-sex-BMI-matched obese non-PWS patients and 7 age-sex-matched lean subjects before and after the administration of 3,139.5 kJ (750 kcal) of a standard liquid meal (53.2% carbohydrate, 30% fat, 16.7% protein) after an overnight fast. Blood samples were obtained every 15 min for the first hour and every 30 min thereafter until 6 h. Adiponectin, IGF-I, glucose, triglycerides, cholesterol, and insulin were measured. Results:Fasting plasma adiponectin levels were lower in PWS than in lean subjects (5.24 ± 2.56 vs. 8.28 ± 4.63 µg/ml, p = 0.041) but higher than in obese patients (4.01 ± 1.27 µg/ml, p = 0.047). After the meal, adiponectin concentrations mildly decreased in PWS at time point 240 min, while in obese and lean subjects no changes were observed. However, 6-hour postprandial AUC for adiponectin was similar in all three groups. Conclusion: Fasting adiponectin levels are low in PWS, but they are so mildly modulated postprandially that these changes do not seem significant for the pathogenesis of obesity in this syndrome.
ISSN:1663-2818
0301-0163
1663-2826
DOI:10.1159/000090513