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DHEA does not bind to or activate the progesterone, glucocorticoid, or mineralocorticoid receptors. [19] [24] Other nuclear receptor targets of DHEA besides the androgen and estrogen receptors include the PPARα, PXR, and CAR. [25] However, whereas DHEA is a ligand of the PPARα and PXR in rodents, it is not in humans. [26]
DHEA and DHEA-S are the most abundant circulating steroids in the body. [29] Plasma levels of DHEA-S are 100 or more times higher than those of DHEA, 5 to 10 times higher than those of cortisol, 100 to 500 times those of testosterone, and 1,000 to 10,000 times higher than those of estradiol. [30] [3] Levels of DHEA and DHEA-S vary throughout life.
Dehydroepiandrosterone (DHEA), DHEA sulfate (DHEA-S), and androstenedione may all be considered proandrogens of testosterone. [ 1 ] In the last two decades, prohormones have also been used by bodybuilders, athletes, and nonmedical users of AAS and other hormones to refer to substances that are expected to convert to active hormones in the body.
The 1999 study mentioned earlier found that DHEA didn’t increase testosterone levels in participants when they took 50 milligrams of DHEA daily for six months. And the pooled analysis found that ...
Androstenedione, or 4-androstenedione (abbreviated as A4 or Δ 4-dione), also known as androst-4-ene-3,17-dione, is an endogenous weak androgen steroid hormone and intermediate in the biosynthesis of estrone and of testosterone from dehydroepiandrosterone (DHEA). It is closely related to androstenediol (androst-5-ene-3β,17β-diol).
Dihydrotestosterone (DHT) is a metabolite of testosterone, and a more potent androgen than testosterone in that it binds more strongly to androgen receptors. It is produced in the skin and reproductive tissue. A4 and testosterone can also have an extra hydroxyl (-OH) or keton (=O) group bound on position 11.