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G蛋白偶联受体54与青春期。

GPR54 and puberty.

作者信息

Colledge William H

机构信息

Physiology Department, University of Cambridge, Cambridge, CB2 3EG, UK.

出版信息

Trends Endocrinol Metab. 2004 Nov;15(9):448-53. doi: 10.1016/j.tem.2004.09.008.

DOI:10.1016/j.tem.2004.09.008
PMID:15519892
Abstract

At puberty, pulsatile secretion of hormones initiates sexual maturation of the gonads. The G-protein-coupled receptor GPR54 is crucially involved in the initiation of puberty, along with its ligand metastin. Mice lacking GPR54 fail to undergo puberty and have immature reproductive organs and low levels of sex steroids and gonadotrophic hormones, but have normal levels of gonadotrophin-releasing hormone in the hypothalamus. In humans, several cases of hypogonadism have been ascribed to mutations in GPR54. Production of metastin and, to a lesser extent, GPR54 are negatively regulated by testosterone and oestrogen, and injecting GPR54 ligands can increase hormone secretion in rodents. Thus, GPR54 is required for normal functioning of the hypothalamic-pituitary-gonadal axis, probably at the level of gonadotrophin-releasing-hormone secretion.

摘要

在青春期,激素的脉冲式分泌启动性腺的性成熟。G蛋白偶联受体GPR54与其配体促性腺素释放肽一起,在青春期启动过程中起关键作用。缺乏GPR54的小鼠无法进入青春期,其生殖器官不成熟,性类固醇和促性腺激素水平较低,但下丘脑促性腺激素释放激素水平正常。在人类中,几例性腺功能减退病例被归因于GPR54的突变。促性腺素释放肽的产生以及程度较轻的GPR54的产生受到睾酮和雌激素的负调控,向啮齿动物注射GPR54配体可增加激素分泌。因此,GPR54是下丘脑-垂体-性腺轴正常功能所必需的,可能是在促性腺激素释放激素分泌水平上。

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