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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone and Men's Health Articles
Advances in stem cell research for the treatment of primary hypogonadism
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<blockquote data-quote="madman" data-source="post: 209435" data-attributes="member: 13851"><p><strong>Fig. 2 | The development of human Leydig cells. a | Fetal Leydig cells (FLCs) are cells that produce testosterone before birth. They originate from the mesenchymal cells present in the mesonephros, coelomic epithelial (CE) cells, neural crest cells (NCC), or cells present in the adrenogonadal primordium (AGP). The precursors of FLCs, such as mesenchymal cells expressing steroidogenic factor 1 (SF-1), migrate into the gonads and form FLCs. b| Some cells present in the mesonephros differentiate into testicular mesenchymal cells (TMCs), which continue to proliferate or are at rest until the postnatal age. At the postnatal age of 2 months, a second wave of testosterone is produced by neonatal Leydig cells (NLCs), which are derived from either non-degraded FLCs or newly formed stem Leydig cells (SLCs). After postnatal year 1, NLCs gradually regress. c | Adult Leydig cells (ALCs), which are established during puberty (10–14 years old), are the third developmental stage of human Leydig cells. The differentiation of ALCs is generally divided into four stages, namely SLCs, progenitor Leydig cells (PLCs), immature Leydig cells (ILCs), and ALCs. SLCs originate from non-degraded FLCs, TMCs, peritubular cells located on the outer face of seminiferous tubules, or perivascular cells associated with testicular blood vessels. 3β-HSD, 3β-hydroxysteroid dehydrogenase; 17β-HSD, 17β-hydroxysteroid dehydrogenase/ketosteroid reductase; CYP11A1, cholesterol side-chain cleavage enzyme, mitochondrial; CYP17A1, steroid 17α-hydroxylase/17,20 lyase.</strong></p><p><strong>[ATTACH=full]16856[/ATTACH]</strong></p></blockquote><p></p>
[QUOTE="madman, post: 209435, member: 13851"] [B]Fig. 2 | The development of human Leydig cells. a | Fetal Leydig cells (FLCs) are cells that produce testosterone before birth. They originate from the mesenchymal cells present in the mesonephros, coelomic epithelial (CE) cells, neural crest cells (NCC), or cells present in the adrenogonadal primordium (AGP). The precursors of FLCs, such as mesenchymal cells expressing steroidogenic factor 1 (SF-1), migrate into the gonads and form FLCs. b| Some cells present in the mesonephros differentiate into testicular mesenchymal cells (TMCs), which continue to proliferate or are at rest until the postnatal age. At the postnatal age of 2 months, a second wave of testosterone is produced by neonatal Leydig cells (NLCs), which are derived from either non-degraded FLCs or newly formed stem Leydig cells (SLCs). After postnatal year 1, NLCs gradually regress. c | Adult Leydig cells (ALCs), which are established during puberty (10–14 years old), are the third developmental stage of human Leydig cells. The differentiation of ALCs is generally divided into four stages, namely SLCs, progenitor Leydig cells (PLCs), immature Leydig cells (ILCs), and ALCs. SLCs originate from non-degraded FLCs, TMCs, peritubular cells located on the outer face of seminiferous tubules, or perivascular cells associated with testicular blood vessels. 3β-HSD, 3β-hydroxysteroid dehydrogenase; 17β-HSD, 17β-hydroxysteroid dehydrogenase/ketosteroid reductase; CYP11A1, cholesterol side-chain cleavage enzyme, mitochondrial; CYP17A1, steroid 17α-hydroxylase/17,20 lyase. [ATTACH type="full"]16856[/ATTACH][/B] [/QUOTE]
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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone and Men's Health Articles
Advances in stem cell research for the treatment of primary hypogonadism
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