Adiponectin orchestrates testosterone suppression in biological pathways

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.