Free and total leptin serum levels and soluble leptin receptors levels in two models of genetic obesity: the Prader-Willi and the Down syndromes

• Published in: Metabolism, clinical and experimental clinical and experimental, 2007-08, Vol.56 (8), p.1076-1080
• Main Authors: Proto, Caterina, Romualdi, Daniela, Cento, Rosa Maria, Romano, Corrado, Campagna, Giuseppe, Lanzone, Antonio
• Format: Article
• Language: English
• Subjects: Adult; Biological and medical sciences; Chromosome aberrations; Complex syndromes; Down Syndrome - blood; Down Syndrome - complications; Down Syndrome - genetics; Endocrinology & Metabolism; Female; Hormones - blood; Humans; Leptin - blood; Medical genetics; Medical sciences; Metabolic diseases; Obesity; Obesity - blood; Obesity - etiology; Obesity - genetics; Prader-Willi Syndrome - blood; Prader-Willi Syndrome - complications; Prader-Willi Syndrome - genetics; Radioimmunoassay; Receptors, Cell Surface - blood; Receptors, Leptin
• ISSN: 0026-0495; 1532-8600
• DOI: 10.1016/j.metabol.2007.03.016

Abstract Alterations in energy balance and feeding behavior and the subsequent high frequency of obesity are hallmarks of 2 chromosomal diseases: the Prader-Willi syndrome (PWS) and the Down syndrome (DS). Leptin, an important regulator of food intake and energy homeostasis, circulates in 2 forms: a free, therefore active, fraction and a fraction bound to the soluble leptin receptor, whose bioavailability consequently participates in the regulation of leptin action. To investigate the possible role of the free-bound leptin balance in the pathogenesis of obesity in PWS and DS, we enrolled 7 obese women with DS, 5 obese women with PWS, 7 obese women, and 7 normal-weight healthy control women. Basal hormonal concentrations, total and free leptin levels, and leptin receptors levels were measured in plasma samples obtained from the 4 groups. No significant differences were observed in the hormonal milieu. Women with DS exhibited lower total leptin concentrations ( P < .01), comparable leptin receptor level and, therefore, lower free leptin values ( P < .01) when compared with obese controls, then resembling the profile peculiar to normal-weight control women. At variance, subjects with PWS did not differ from obese controls regarding both leptin and leptin receptor levels. Our data suggest that, whereas subjects with PWS have a leptin assessment corresponding to their degree of obesity, subjects with DS may have a defect in the secretion of leptin that could at least partially account for this form of syndromal obesity.