Altered regulation of adrenal steroidogenesis in @entity1300 -treated XXXX .

@entity2819 @entity23 @entity3317 @entity35 @entity1300 @entity7816 @entity165
A single treatment of @entity1300 ( @entity1300 ) (50 micrograms/kg) produced two distinct effects on adrenal steroidogenesis in @entity35 13 days post-treatment. In unstressed @entity35 , the very low @entity2819 levels early in the light phase (AM) increased 4-fold relative to @entity23 ( @entity23 ) @entity35 , but the peak level of @entity2819 that is seen late in the light phase (PM) decreased up to 40% relative to @entity23 @entity35 . The AM stimulation was also observed in @entity35 pair-fed to compensate for the diminished feed intake of @entity1300 -treated animals, indicating that the change results from nutritional deprivation. The PM suppression, however, was not observed in pair-fed @entity35 . In @entity35 given a lower dose of @entity1300 (15 micrograms/kg), there was no AM stimulation, whereas the suppression of the PM diurnal peak of @entity2819 was retained. Plasma @entity3317 (ACTH) levels and adrenal size were not changed by these treatments, indicating that @entity1300 affects adrenal responsiveness. @entity1300 did not, however, have a significant effect on @entity2819 secretion in @entity35 receiving high doses of ACTH. In control animals, the availability of @entity165 to @entity7816 limits the rate of steroidogenesis. While the specific content of the cytochrome was unaffected by @entity1300 , @entity165 turnover by this enzyme appeared to be affected following @entity1300 treatment, as evidenced by small increases in the mitochondrial levels of free @entity165 , reactive @entity165 , and in the proportion of @entity7816 complexed with @entity165 relative to both ad libitum- and pair-fed controls. This accumulation of mitochondrial @entity165 following @entity1300 treatment is consistent with an inhibition of @entity165 metabolism at @entity7816 in vivo that is removed upon isolation of the mitochondria. These @entity1300 -induced increases were enhanced substantially in ACTH-stimulated @entity35 , probably because ACTH enhances @entity165 influx into the mitochondria. Normally, substrate availability is rate limiting in @entity165 side-chain cleavage, and the AM stimulation of steroidogenesis by @entity1300 may result from such increased @entity165 transfer. The inhibition of @entity165 side-chain cleavage resulting from @entity1300 treatment may, however, only become rate limiting for @entity2819 synthesis when @entity165 transfer is more substantially activated, as for peak PM secretion.
