Shintani M, Ogawa Y, Nakao K
Department of Medicine and Clinical Science, Kyoto University Graduate School of Medical.
Nihon Rinsho. 2000 Feb;58(2):327-32.
Leptin, the obese gene product, is an adipocyte-derived satiety factor which is involved in the regulation of food intake and energy expenditure. Obesity often accompanies insulin resistance and high levels of leptin. In in vitro studies, leptin has been reported to increase fatty acid oxidation and decrease fatty acid synthesis in adipocytes and hepatocytes. The direct effects of leptin on glucose metabolism and insulin signaling have not been clarified yet. In in vivo studies, however, leptin has been reported to improve insulin sensitivity and glucose metabolism in normal and obese rodents acting mainly through hypothalamus. Moreover leptin has been reported to have antidiabetic effects in insulin-deficient diabetes rats and lipoatrophic diabetes mice. It is suggested that leptin modulates insulin sensitivity and glucose disposal and that leptin may have a pathophysiological and therapeutic implications in diabetes.
瘦素是肥胖基因的产物,是一种由脂肪细胞产生的饱腹感因子,参与食物摄入和能量消耗的调节。肥胖常伴有胰岛素抵抗和高瘦素水平。在体外研究中,据报道瘦素可增加脂肪细胞和肝细胞中的脂肪酸氧化并减少脂肪酸合成。瘦素对葡萄糖代谢和胰岛素信号传导的直接影响尚未阐明。然而,在体内研究中,据报道瘦素主要通过下丘脑作用,可改善正常和肥胖啮齿动物的胰岛素敏感性和葡萄糖代谢。此外,据报道瘦素对胰岛素缺乏型糖尿病大鼠和脂肪萎缩性糖尿病小鼠具有抗糖尿病作用。提示瘦素可调节胰岛素敏感性和葡萄糖处置,并且瘦素可能在糖尿病中具有病理生理学和治疗意义。