Cento R M, Proto C, Spada R S, Ragusa L, Reitano S, Napolitano V, Lanzone A
Unit of Obstetrics and Gynecology, OASI Institute for Research (IRCCS), Troina, Italy.
Gynecol Endocrinol. 1999 Feb;13(1):36-41. doi: 10.1080/09513599909167529.
We have evaluated serum leptin concentrations in two forms of genetic obesity. The subjects examined were eight women with Down syndrome and eight women with Prader-Willi syndrome. All patients were in the reproductive age range and were obese (body mass index > or = 27 kg/m2). Plasma leptin values, analyzed as a function of body mass index showed a statistically significant correlation in both Prader-Willi (r = 0.985; p < 0.001) and Down syndrome patients (r = 0.943; p < 0.001). Obese Down syndrome women exhibited significantly lower leptin values (10.8 +/- 1.1) as compared to patients with Prader-Willi syndrome (31 +/- 2.6; p < 0.01). The linear correlation between leptin and insulin in the two groups of patients was not statistically significant. The data suggested that obesity in Prader-Willi subjects could be caused by failure of leptin to reach its target in the brain, as a consequence of defects in the receptor or in postreceptor processing, whereas data on obese patients with Down syndrome could be due to a different pathogenetic origin.
我们评估了两种遗传性肥胖患者的血清瘦素浓度。研究对象为8名唐氏综合征女性和8名普拉德-威利综合征女性。所有患者均处于生育年龄且肥胖（体重指数≥27kg/m²）。将血浆瘦素值作为体重指数的函数进行分析，结果显示普拉德-威利综合征患者（r = 0.985；p < 0.001）和唐氏综合征患者（r = 0.943；p < 0.001）的瘦素值与体重指数均存在统计学显著相关性。与普拉德-威利综合征患者（31±2.6；p < 0.01）相比，肥胖的唐氏综合征女性的瘦素值显著更低（10.8±1.1）。两组患者中瘦素与胰岛素之间的线性相关性无统计学意义。数据表明，普拉德-威利综合征患者的肥胖可能是由于瘦素无法到达大脑中的靶点，这是受体或受体后加工缺陷的结果，而唐氏综合征肥胖患者的数据可能归因于不同的发病机制。
