Cohen B, Novick D, Rubinstein M
Department of Molecular Genetics, The Weizmann Institute of Science, Rehovot 76100, Israel.
Science. 1996 Nov 15;274(5290):1185-8. doi: 10.1126/science.274.5290.1185.
Leptin mediates its effects on food intake through the hypothalamic form of its receptor OB-R. Variants of OB-R are found in other tissues, but their function is unknown. Here, an OB-R variant was found in human hepatic cells. Exposure of these cells to leptin, at concentrations comparable with those present in obese individuals, caused attenuation of several insulin-induced activities, including tyrosine phosphorylation of the insulin receptor substrate-1 (IRS-1), association of the adapter molecule growth factor receptor-bound protein 2 with IRS-1, and down-regulation of gluconeogenesis. In contrast, leptin increased the activity of IRS-1-associated phosphatidylinositol 3-kinase. These in vitro studies raise the possibility that leptin modulates insulin activities in obese individuals.
瘦素通过其受体OB-R的下丘脑形式介导其对食物摄入的影响。OB-R的变体存在于其他组织中,但其功能尚不清楚。在这里,在人肝细胞中发现了一种OB-R变体。将这些细胞暴露于与肥胖个体中存在的浓度相当的瘦素中,会导致几种胰岛素诱导的活性减弱,包括胰岛素受体底物-1(IRS-1)的酪氨酸磷酸化、衔接分子生长因子受体结合蛋白2与IRS-1的结合以及糖异生的下调。相比之下,瘦素增加了与IRS-1相关的磷脂酰肌醇3-激酶的活性。这些体外研究提出了瘦素调节肥胖个体胰岛素活性的可能性。