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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone and Men's Health Articles
Leydig cell aging: Molecular mechanisms and treatments
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<blockquote data-quote="madman" data-source="post: 209084" data-attributes="member: 13851"><p><strong>Fig. 1 <u>Cell biology of Leydig cell T formation</u>. LH binds its receptor on the Leydig cell membrane. LH receptor/G protein coupling results in increased cAMP production. cAMP stimulates the mobilization and transport of cholesterol to and into the mitochondria in part by activating cAMP-dependent protein kinase (PKA). Free cholesterol for steroidogenesis originates from various intracellular locations, including the plasma membrane, endoplasmic reticulum, and lipid droplets. LH binding to LC plasma membrane receptors induces the formation of a supramolecular complex of cytosolic and mitochondrial proteins, referred to as the Steroidogenic InteracTomE (SITE). Cholesterol movement into mitochondria is accomplished by a series of protein-protein interactions at SITE ending at active site of CYP11A1 in the matrix side of IMM. Cholesterol is converted to pregnenolone by CYP11A1, pregnenolone is converted into progesterone by enzymes present in mitochondria and endoplasmic reticulum (3βHSD), and progesterone is metabolized to T by enzymes exclusively present in the endoplasmic reticulum (CYP17A1 and 17βHSD).</strong></p><p><strong>[ATTACH=full]16795[/ATTACH]</strong></p></blockquote><p></p>
[QUOTE="madman, post: 209084, member: 13851"] [B]Fig. 1 [U]Cell biology of Leydig cell T formation[/U]. LH binds its receptor on the Leydig cell membrane. LH receptor/G protein coupling results in increased cAMP production. cAMP stimulates the mobilization and transport of cholesterol to and into the mitochondria in part by activating cAMP-dependent protein kinase (PKA). Free cholesterol for steroidogenesis originates from various intracellular locations, including the plasma membrane, endoplasmic reticulum, and lipid droplets. LH binding to LC plasma membrane receptors induces the formation of a supramolecular complex of cytosolic and mitochondrial proteins, referred to as the Steroidogenic InteracTomE (SITE). Cholesterol movement into mitochondria is accomplished by a series of protein-protein interactions at SITE ending at active site of CYP11A1 in the matrix side of IMM. Cholesterol is converted to pregnenolone by CYP11A1, pregnenolone is converted into progesterone by enzymes present in mitochondria and endoplasmic reticulum (3βHSD), and progesterone is metabolized to T by enzymes exclusively present in the endoplasmic reticulum (CYP17A1 and 17βHSD). [ATTACH type="full"]16795[/ATTACH][/B] [/QUOTE]
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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone and Men's Health Articles
Leydig cell aging: Molecular mechanisms and treatments
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