Niimi M
Department of Clinical Laboratory Medicine, Kagawa Medical University.
Nihon Rinsho. 2001 Mar;59(3):443-8.
Leptin inhibits food intake and increase energy expenditure via an interaction with specific leptin receptors located in the hypothalamus. Leptin receptors have been identified in cocaine and amphetamine-regulated transcript(CART), neuropeptide Y(NPY), galanin-containing neurons of the arcuate nucleus, respectively, and in corticotropin-releasing hormone(CRH)-containing neurons of the paraventricular nucleus, suggesting that these peptides are mediators of leptin's action in the hypothalamus. Anabolic pathways such as those including NPY and galanin promote feeding and are inhibited by leptin, whereas catabolic pathways which include CART and CRH have the opposite effect and are stimulated by leptin. In the current review we examine the significant role of the CART, CRH, NPY and galanin in the regulation of energy balance.
瘦素通过与位于下丘脑的特定瘦素受体相互作用来抑制食物摄入并增加能量消耗。已分别在弓状核的可卡因和苯丙胺调节转录物(CART)、神经肽Y(NPY)、含甘丙肽的神经元中以及室旁核的含促肾上腺皮质激素释放激素(CRH)的神经元中鉴定出瘦素受体,这表明这些肽是瘦素在下丘脑中作用的介质。诸如包括NPY和甘丙肽的那些合成代谢途径促进进食并受到瘦素的抑制,而包括CART和CRH的分解代谢途径则具有相反的作用并受到瘦素的刺激。在本综述中,我们研究了CART、CRH、NPY和甘丙肽在能量平衡调节中的重要作用。