An Adaptation of Testosterone Release to Hypoxia

Kai-Lee Wang ； Yu-Min Cho ； Shyi-Wu Wang ； Paulus S. Wang

《Adaptive Medicine》 11卷4期 (2019/12) Pp. 113-115

https://doi.org/10.4247/AM.2019.ABJ237

摘要

Oxygen homeostasis is an essential issue for human being to survival. Hypoxia is defined as the oxygen deficiency in a habitat or a body part. Previous studies have demonstrated that hypoxia plays a critical role in testosterone (T) biosynthesis but the effects and mechanisms still remain controversial. In our previous study, we found that T and vascular endothelial growth factor (VEGF) levels were increased in a mouse TM3 Leydig cell line after hypoxia treatment. TM3 cell proliferation was also found. Moreover, the T release was stimulated after VEGF treatment in a dose-dependent manner. The stimulatory effect of VEGF on T release was abolished after anti-VEGF antibody treatment. In a recent paper published in Life Science, we demonstrated that the plasma T levels as well as testicular microvasculature VEGF levels were both increased in the chronic intermittent hypoxia (12% O_2, 8 hours/day for 14 days, CIH) group. Furthermore, luteinizing hormone (LH) receptor expression, testicular angiogenesis, CYP11A1 activity, 17β-hydroxysteroid dehydrogenase (HSD) activity, and calcium-related pathway were all elevated after CIH treatment. This research affords a new method and mechanism into the study of testosterone release. These results suggested that hypoxia stimulated T biosynthesis in adult Leydig cells, at least partly, through increase of the sensitivity in response to LH and enzyme activity.

關鍵字

chronic intermittent hypoxia ； Leydig cell ； testosterone ； luteinizing hormone receptor ； CYP11A1 (P450scc) ； steroidogenesis