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#testosterone

8 public questions tagged with this topic.

Sex determination-l

Which hormone converts testosterone into dihydrotestosterone (DHT)?

Conversion of testosterone into more potent dihydrotestosterone responsible for external genital masculinization is catalyzed not by hormone but by membrane enzyme steroid 5α-reductase type 2 encoded by SRD5A2 gene. Enzyme localized in genital skin, prostate and hair follicles uses NADPH to reduce testosterone double bond forming DHT. DHT binds androgen receptor with higher affinity and slower dissociation ensuring robust activation of male morphogenetic genes. Confusing hormone with enzyme is common, but catalytic step essential. In provided options intended catalyst for external genitalia virilization corresponds to 5α-reductase activity.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 17: 5α-reductase converts testosterone to DHT.

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Sex determination-l

Leydig cells in mammals produce:

Leydig cells originate from mesenchymal progenitors in interstitial compartment under Desert hedgehog signaling from Sertoli cells and transcription factor Sf1. They express steroidogenic acute regulatory protein and enzymes Cyp11a1, Hsd3b1, Cyp17a1 converting cholesterol to testosterone. Their principal product testosterone secreted in fetal life stabilizes Wolffian ducts differentiating into seminal vesicles, epididymis and vas deferens, supports masculinization of brain and later promotes spermatogenesis. Testosterone also serves as precursor for dihydrotestosterone in external genitalia and estradiol in brain. Insufficient function causes female phenotype.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 17: Leydig cells produce testosterone in fetal testis.

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sex determination-ll

Hormone promoting male genitalia:

Male external genitalia differentiation depends predominantly on dihydrotestosterone acting via androgen receptor in genital tubercle and swellings. While testosterone maintains Wolffian duct derivatives, DHT binding induces conformational change stabilizing androgen receptor dimer that translocates to nucleus and binds androgen response elements regulating morphogenetic genes. DHT drives elongation of tubercle forming penis, canalization of urethra by fusion of urogenital folds, and formation of scrotum from labioscrotal swellings. Loss-of-function of 5α-reductase or receptor results in feminized external genitalia despite male internal anatomy, proving DHT critical.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 17: DHT drives male external genitalia differentiation.

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sex determination-ll

Enzyme converting testosterone into DHT:

Development of male external genitalia requires local conversion of testosterone secreted by Leydig cells into more active androgen dihydrotestosterone. Reaction catalyzed by microsomal enzyme steroid 5α-reductase type 2 encoded by SRD5A2 gene which uses NADPH to reduce Δ4-5 double bond. DHT exhibits higher affinity for androgen receptor and prolonged receptor-DNA interaction, activating genes for penile growth, urethral closure and scrotal fusion. Deficiency of enzyme causes pseudovaginal perineoscrotal hypospadias despite normal Wolffian ducts, while aromatase converts testosterone to estradiol irrelevant for this masculinization.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 17: 5α-reductase converts testosterone to DHT.

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