Arai K, Shibasaki T
Department of Physiology, Nippon Medical School.
Nihon Rinsho. 2001 Mar;59(3):449-55.
Recently, leptin was cloned and characterized as a sateity factor which acts through the hypothalamus. alpha-melanocyte-stimulating hormone derived from pro-opiomelanocortin(POMC) and melanocortin receptor-4(MC4-R) have been reported to be involved in the downstream of the effect of leptin. In this paper, we summarized the clinical characteristics and the mechanisms of obesity caused by genetic abnormalities involved in the regulatory mechanism of appetite such as leptin, leptin receptor, POMC, MC4-R and prohormone convertase 1.
最近，瘦素被克隆并被鉴定为一种通过下丘脑起作用的饱足因子。据报道，源自阿片-促黑素皮质素原（POMC）的α-黑素细胞刺激素和黑素皮质素受体-4（MC4-R）参与了瘦素作用的下游过程。在本文中，我们总结了由瘦素、瘦素受体、POMC、MC4-R和激素原转化酶1等食欲调节机制中涉及的基因异常所导致的肥胖的临床特征及机制。
