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. 2020 Jun 30;11:373. doi: 10.3389/fendo.2020.00373

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Copyright © 2020 Barbagallo, Condorelli, Mongioì, Cannarella, Aversa, Calogero and La Vignera.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Leydig cell steroidogenesis. LH binds to its receptors (LHR) on the Leydig cell (LC) membrane. This results in activation of Gs protein and adenylyl cyclase and increased concentration of intracellular cAMP. cAMP stimulates the mobilization and transport of cholesterol within the mitochondria in part by activating PKA and MAPK signaling. The first source of cholesterol for steroidogenesis is via uptake of cholesteryl esters from high-density lipoprotein (HDL) by the scavenger receptor SR-B1. Steroidogenic acute regulatory enzymes (StARs) regulate cholesterol transport from the outer to the inner mitochondrial membrane. At the inner mitochondrial membrane, cholesterol is converted into pregnenolone by CYP11A1 and pregnenolone is converted into testosterone by enzymes in the smooth endoplasmic reticulum (3β-HSD, CYP17A1, and 17β-HSD).