Adiponectin orchestrates testosterone suppression in biological pathways

IF 0.5 Q4 REPRODUCTIVE BIOLOGY
Ekhoye Ehitare Ikekhuamen, Imonna Kingsle
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引用次数: 0

Abstract

This current review highlights adiponectin engagement with AdipoRl and AdipoR2 which subsequently triggers pathways such as AMPK, PPARα, and MAPK, thereby modulating testicular steroidogenesis. Adiponectin's actions on Leydig and adrenal cells inhibit androgen secretion by suppressing the steroidogenic acute regulatory protein (StAR). Given that StAR facilitates cholesterol to testosterone conversion, AMPK inhibits this process by modulating cholesterol transport and suppressing StAR expression through multiple avenues. Furthermore, adiponectin-induced PPARα activation impedes mitochondrial cholesterol influx, further modulating androgen biosynthesis. The suppressive influence of PPARα on steroidogenic genes, notably StAR, is evident. Collectively, adiponectin signalling predominantly attenuates androgen production, ensuring metabolic and reproductive equilibrium. Imbalances, as seen in conditions like hypogonadism and obesity-related infertility, highlight their crucial roles and potential clinical interventions for reproductive disorders.
脂肪连通素在生物通路中协调睾酮抑制作用
本综述重点介绍了脂肪连通素与 AdipoRl 和 AdipoR2 的相互作用,随后触发 AMPK、PPARα 和 MAPK 等通路,从而调节睾丸的类固醇生成。Adiponectin 对 Leydig 和肾上腺细胞的作用是通过抑制类固醇生成急性调节蛋白(StAR)来抑制雄激素分泌。鉴于 StAR 可促进胆固醇向睾酮的转化,AMPK 可通过多种途径调节胆固醇转运并抑制 StAR 的表达,从而抑制这一过程。此外,脂联素诱导的 PPARα 激活会阻碍线粒体胆固醇的流入,从而进一步调节雄激素的生物合成。PPARα 对类固醇生成基因(尤其是 StAR)的抑制作用显而易见。总之,脂肪连通素信号主要抑制雄激素的产生,确保新陈代谢和生殖平衡。性腺功能减退症和肥胖相关性不孕症等疾病中出现的失衡现象凸显了它们的关键作用以及对生殖障碍的潜在临床干预。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Asian Pacific Journal of Reproduction
Asian Pacific Journal of Reproduction Veterinary-Veterinary (all)
CiteScore
1.70
自引率
0.00%
发文量
588
审稿时长
9 weeks
期刊介绍: The journal will cover technical and clinical studies related to health, ethical and social issues in field of Gynecology and Obstetrics. Articles with clinical interest and implications will be given preference.
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