Katsumata N, Tanaka T
Nihon Rinsho. 1997 Nov;55(11):2959-62.
Familial male-limited precocious puberty (FMPP) is a gonadotropin-independent disorder that is inherited in an autosomal dominant, male-limited pattern. Affected males generally exhibit signs of puberty by the age of 4 years. Testosterone production and Leydig cell hyperplasia occur autonomously in context of prepubertal levels of luteinizing hormone (LH). The LH receptor is a member of the family of G-protein-coupled receptors. Thus far, eleven constitutively activating mutations of the LH receptor gene, which result in high basal cyclic AMP levels, have been identified in pedigree with FMPP and in sporadic cases. It has been suggested that some of the mutations have effects on the Gq coupling and phospholipase-C activation in addition to their effects on Gs coupling and activation of adenylate cyclase.
家族性男性限性性早熟(FMPP)是一种不依赖促性腺激素的疾病,以常染色体显性、男性限性模式遗传。受影响的男性通常在4岁时出现青春期体征。在青春期前促黄体生成素(LH)水平的情况下,睾酮的产生和睾丸间质细胞增生自主发生。LH受体是G蛋白偶联受体家族的成员。迄今为止,在患有FMPP的家系和散发病例中,已鉴定出11种LH受体基因的组成性激活突变,这些突变导致基础环磷酸腺苷(cAMP)水平升高。有人提出,除了对Gs偶联和腺苷酸环化酶激活的影响外,一些突变还对Gq偶联和磷脂酶C激活有影响。