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Endocrine-Metabolic Laboratory (C.Pa., A.C., C.Pi., G.M., G.F., R.V.), Department of Medical and Surgical Sciences, Department of Biological Chemistry (O.M., P.S.), and Centro Ricerche Interdipartimentale Biotecnologie Innovative (O.M.), Biotechnology Centre, University of Padua, 35100 Padua, Italy; and Laboratory of Medical Genetics (M.B., E.F., G.A.), Baschirotto Institute for Rare Diseases, Costozza di Longare, 36023 Vicenza, Italy
Address all correspondence and requests for reprints to: Dr. Claudio Pagano, Department of Medical and Surgical Sciences, Via Ospedale 105, 35100 Padova, Italy. E-mail: claudio.pagano{at}unipd.it.
Context: Determinants of insulin resistance in Prader-Willi syndrome (PWS) are not completely understood. The discovery of several adipokines with relevant effects on insulin resistance and cardiovascular complications of metabolic syndrome offered new tools of investigation of insulin resistance in PWS.
Objective: The purpose of this study was to measure serum resistin and mRNA in adipose tissue of patients with PWS, those with simple obesity, and healthy controls and correlate resistin levels with anthropometric and biochemical features.
Design: Twenty-eight adult PWS patients, 29 obese patients, and 25 healthy controls were studied. Anthropometric variables were measured and fasting serum and plasma were collected for measurement of resistin, adiponectin, leptin, lipid profile, glucose, and insulin.
Results: Serum resistin and resistin mRNA expression in adipose tissue was significantly higher in PWS patients, compared with both healthy lean controls and obese patients. Moreover, on regression analysis resistin was significantly correlated with body mass index, whereas no significant association was found between resistin and homeostasis model assessment index. A weak association between resistin and adiponectin was found in the PWS group only. However, on multivariate analysis only the correlation between resistin and body mass index remained significant.
Conclusions: These results support a link between circulating resistin and obesity in humans but do not support a role for resistin in human insulin resistance.
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