Reproductive functions of kisspeptin and Gpr54 across the life cycle of mice and men

被引:29
作者
Chan, Yee-Ming [1 ,2 ,3 ]
Broder-Fingert, Sarabeth [1 ,2 ]
Seminara, Stephanie B. [1 ,2 ]
机构
[1] Massachusetts Gen Hosp, Reprod Endocrine Unit, Boston, MA 02114 USA
[2] Massachusetts Gen Hosp, Harvard Reprod Sci Ctr, Dept Med, Boston, MA 02114 USA
[3] Childrens Hosp, Div Endocrinol, Dept Med, Boston, MA 02115 USA
关键词
GPR54; KISS1; Kisspeptin; Reproduction; Idiopathic hypogonadotropic hypogonadism; IDIOPATHIC HYPOGONADOTROPIC HYPOGONADISM; GONADOTROPIN-RELEASING-HORMONE; ADRENAL HYPOPLASIA CONGENITA; PITUITARY-GONADAL AXIS; KALLMANN-SYNDROME; RECEPTOR GPR54; LUTEINIZING-HORMONE; MUTATIONS; GENE; PHENOTYPES;
D O I
10.1016/j.peptides.2008.06.015
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The reproductive phenotypes of nearly two dozen patients with mutations in GPR54 have been reported, as have the phenotypes of four mouse lines mutant for Gpr54 and two lines mutant for Kiss1. These phenotypes demonstrate that kisspeptin/Gpr54 function is required at all phases of the life cycle when the secretion of gonadotropin-releasing hormone (GnRH) is robust. Furthermore, there is phenotypic variability ranging from severe hypogonadism to partial sexual development. Collectively, these findings suggest that kisspeptin and Gpr54 serve as an essential conduit for relaying developmental information to the GnRH neuron. (C) 2008 Elsevier Inc. All rights reserved.
引用
收藏
页码:42 / 48
页数:7
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