In-vivo changes in steroidogenesis in preantral hamster follicles following exposure to the LH surge could be mimicked by stimulation with exogenous LH in vitro. Luteinizing hormone given only during the first hour (media were changed every hour) of a 6-h incubation promptly increased the concentration of androstenedione and adenosine 3′:5′-monophosphate (cAMP) in the media and this was followed by a gradual decline to <20% of the peak value; progesterone in media was not detectable with a single LH stimulation. However, LH given every hour increased progesterone and cAMP concentrations in the media throughout the period of incubation, but the transient increase and subsequent decline in androstenedione was still observed. The decline in androstenedione release by preantral follicles was apparently due to a lack of steroid precursor and not to either inhibition of hydroxyl-lyase or lack of LH or cAMP stimulation. Exogenous dibutyryl cAMP (dbcAMP) and 8-Br-cAMP mimicked the effects of LH on the pattern of follicular androstenedione release into the media; however, dbcAMP and 8-Br-cAMP did not increase concentrations of progesterone in vitro. In preantral follicles, LH stimulated cAMP release into the media and apparently inhibited phosphodiesterase activity, since methyl isobutylxanthine (MIX) did not potentiate the effect of LH on cAMP. Follicle-stimulating hormone also increased androstenedione and cAMP in the media of the preantral follicles in a manner similar to that of LH, except that between 4 and 6 h of incubation the release of androstenedione and cAMP was less than that produced by stimulation with LH. Interestingly, FSH and MIX stimulated androstenedione and cAMP release by preantral follicles in a manner similar to that induced by LH alone.
These results indicate that LH stimulation of preantral follicles in vitro induces an androstenedione– progesterone shift which is mediated by cAMP. The decline in androstenedione release by the preantral follicle in vitro appears to be due to a lack of appropriate steroid precursors and not to an inhibitory action of LH on androgen synthesis.
J. Endocr. (1987) 114, 55–63
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