Sechenov Institute of Evolutionary Physiology and Biochemistry, Russian Academy of Sciences, St. Petersburg, Russia.
Bull Exp Biol Med. 2024 Aug;177(4):436-441. doi: 10.1007/s10517-024-06204-x. Epub 2024 Sep 12.
We studied the effect of a high-fat, high-carbohydrate diet (HFHCD) on basal testosterone levels in the blood and testosterone, its precursors, and expression of steroidogenic genes in the testes of rats treated with human chorionic gonadotropin (hCG, 10 IU/rat, subcutaneously, once), gonadotropin-releasing hormone receptor antagonist cetrorelix (75 μg/kg, subcutaneously, 3 days), and their combination. In HFHCD rats, no obvious signs of androgen deficiency were observed and the response of the testes to hCG stimulation was preserved. Unlike control rats (normal diet), the expression of the luteinizing hormone receptor gene in these rats did not change in response to hCG stimulation and cetrorelix administration; they also showed a paradoxical, more pronounced response to hCG administration under conditions of suppression of the gonadotropin secretion by cetrorelix. This suggests that the etiology and pathogenesis of obesity may have different effects on the hormonal status of the male reproductive system.
我们研究了高脂肪、高碳水化合物饮食（HFHCD）对接受人绒毛膜促性腺激素（hCG，10 IU/大鼠，皮下，一次）、促性腺激素释放激素受体拮抗剂 cetrorelix（75 μg/kg，皮下，3 天）治疗的大鼠血液基础睾酮水平以及睾丸中睾酮、其前体和类固醇生成基因表达的影响。在 HFHCD 大鼠中，没有观察到明显的雄激素缺乏迹象，并且睾丸对 hCG 刺激的反应得到保留。与对照大鼠（正常饮食）不同，这些大鼠的黄体生成素受体基因的表达对 hCG 刺激和 cetrorelix 给药没有反应；它们还表现出对 hCG 给药的反常、更明显的反应，在 cetrorelix 抑制促性腺激素分泌的情况下。这表明肥胖的病因和发病机制可能对男性生殖系统的激素状态有不同的影响。
