Kühn-Velten N, Codjambopoulo P, Haider S G, Passia D, Kley H K, Herberg L, Staib W, Goslar H G
Int J Androl. 1986 Apr;9(2):123-31. doi: 10.1111/j.1365-2605.1986.tb00875.x.
Male C57Bl/6J-ob/ob mice (4 months old) and their homozygous lean controls were compared with respect to pituitary LH secretion and functional parameters of purified Leydig cells in vitro. Compared with controls, obese mice showed reductions in the following parameters: Plasma testosterone levels (reduced by 57%), hCG-stimulated testosterone formation in vitro (by 31%), conversion of progesterone to androgens by Leydig cells (by 39%), and GnRH-stimulated LH secretion (by 26%). Lipid accumulation and a 37% decrease in naphthylesterase activity in the Leydig cells as well as hyperplasia of pituitary gonadotrophs were observed histochemically in obese mice. The changes in testicular endocrine function in obese mice are interpreted as consequences of pituitary dysfunction.
将4月龄雄性C57Bl/6J-ob/ob小鼠及其纯合瘦型对照在垂体促黄体生成素(LH)分泌以及体外纯化睾丸间质细胞功能参数方面进行了比较。与对照相比,肥胖小鼠的以下参数降低:血浆睾酮水平(降低57%)、体外人绒毛膜促性腺激素(hCG)刺激的睾酮生成(降低31%)、睾丸间质细胞将孕酮转化为雄激素的能力(降低39%)以及促性腺激素释放激素(GnRH)刺激的LH分泌(降低26%)。在肥胖小鼠中,通过组织化学观察到睾丸间质细胞中脂质蓄积、萘酯酶活性降低37%以及垂体促性腺细胞增生。肥胖小鼠睾丸内分泌功能的变化被解释为垂体功能障碍的结果。