Dihydrotestosterone, commonly abbreviated as DHT, is a potent androgen hormone synthesized primarily from testosterone by the enzyme 5-alpha reductase in peripheral tissues like the prostate, skin, and hair follicles. This highly active metabolite binds to the androgen receptor with greater affinity than testosterone, mediating many of the hormone’s critical effects on male sexual differentiation and secondary sexual characteristics. Elevated or deficient DHT levels can have significant clinical consequences for prostate health, hair growth, and overall androgenic signaling.
Origin
The term is a chemical name combining “di-” (two), “hydro-” (hydrogen), and “testosterone,” indicating a molecular structure that is a reduced form of testosterone. The abbreviation “DHT” is standard clinical and scientific shorthand. Its biological significance was established with the discovery of the 5-alpha reductase enzyme and its role in converting testosterone into this more potent form.
Mechanism
The primary mechanism of action for DHT involves its local conversion from testosterone, which then acts as a potent agonist at the androgen receptor (AR) within target cells. This binding initiates signal transduction, leading to the transcription of specific genes that mediate its biological effects, such as promoting prostate growth and inducing male pattern hair loss in genetically susceptible individuals. Unlike testosterone, DHT is not a substrate for the aromatase enzyme, meaning it cannot be converted directly into estrogen, which contributes to its distinct physiological profile.
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