Evidence that Testosterone Regulates Leydig Cell 3β‐Hydroxysteroid Dehydrogenase‐Isomerase Activity by a Trans‐Acting Factor Distal to the Androgen Receptor

摘要: Leydig cells are a target for their own steroid product, testosterone, and thus could be subject to short-loop feedback regulation by androgens. The authors previously reported that 3 beta-hydroxysteroid dehydrogenase-isomerase (3 beta HSD) activity was higher in freshly isolated from C57BL/6J than those C3H/HeJ inbred mice. To determine whether this strain-related difference HSD mediated differential sensitivity effects of the two strains were cultured presence or absence synthetic androgen receptor agonist, mibolerone, nonaromatizable androgen, dihydrotestosterone. After 7 days treatment, all three androgens significantly decreased C57BL/6J, but not When with hydroxyflutamide, an antagonist, effect testosterone negated. protein, reciprocal F1 hybrid lines mice testosterone. Testosterone treatment inhibited both same extent as observed Thus, there is response it cannot account cell because high strain (C57BL/6J) sensitive strain. Although on receptor-mediated, dominant rules out protein per se. However, data consistent being trans-acting factor distal receptor.