ABSTRACT
After the administration of anabolic steroids to adult female rats in daily doses of 1 mg per animal for 14 days, the following parameters were investigated: the rate of the Δ4-5α-hydrogenase-catalyzed cortisone reduction in liver slices and microsomal fractions, the adrenal weight and the in vitro corticosterone production rate.
Among the steroids tested, only 17α-methyl-testosterone and 17α-ethyl-19-nor-testosterone were effective in lowering significantly cortisone reduction rate by liver slices with concomitant decreases in microsomal Δ4-5α-hydrogenase-activity. Testosterone, 19-nor-testosterone, 17α-ethinyl-19-nor-testosterone, 17α-methyl-17β-hydroxy-androsta-1,4-dien-3-one and 1-methyl-17β-hydroxy-androst-1-en-3-one were ineffective or only slightly effective.
Adrenal weight and absolute corticosterone production rate (μg/60 min per animal) were decreased after treatment with 17α-methyl-testosterone, 17α-ethyl-19-nor-testosterone and 1-methyl-17β-hydroxy-androst-1-en-3-one. Corticosterone production was decreased with 17α-ethinyl-19-nor-testosterone in spite of an unchanged adrenal weight. The relative corticosterone production rate (μg/60 min · 100 mg adrenal) was in any cases unaffected.
According to these results there exists – with the exception of 17α-ethinyl-19-nor-testosterone – a strict parallelism between corticosteroid turnover and corticosterone production rate: unchanged turnover is correlated with unchanged corticosterone production rate, while a decreased turnover is correlated with decreased adrenal activity.
The protein-anabolic effect of certain anabolic steroids may be partly due to an anti-catabolic action of these compounds resulting from a decreased corticosteroid inactivation and production rate.
Possible mechanisms by which anabolic steroids may affect corticosteroid-balance are discussed.
Vitamin B6 deficiency disrupts serotonin signaling in pancreatic islets and induces gestational diabetes in mice
