Related Experiment Videos
Postovulatory decrease in estrogen production is caused by the diminished supply of aromatizable androgen to ovarian
Abstract:
After administration of testosterone to immature rats which had ovulated after treatment with PMSG and hCG, a significant increase in ovarian content of estradiol-17 beta was observed. Together with our previous result on the immediate decrease in ovarian 17 alpha-hydroxylase and C-17-C-20 lyase after PMSG and hCG treatment, it is concluded that the drastic decrease in serum estradiol-17 beta after ovulation is caused by a shortage of supply of aromatizable androgen(s) to the ovarian aromatase, due to diminished activities of the above two enzymes.
Insights
Testosterone administration increased ovarian estradiol-17 beta in rats. This suggests that reduced activity of key enzymes, not aromatase supply, limits estradiol production after ovulation.
Area of Science:
- Reproductive endocrinology
- Steroidogenesis
- Hormonal regulation of ovulation
Background:
- Ovulation is triggered by gonadotropins like PMSG and hCG.
- Estradiol-17 beta levels decrease significantly after ovulation.
- Ovarian enzymes 17 alpha-hydroxylase and C17-C20 lyase activity is affected by gonadotropin treatment.
Purpose of the Study:
- To investigate the effect of testosterone administration on ovarian estradiol-17 beta content in immature rats post-ovulation.
- To elucidate the role of ovarian androgen supply in regulating estradiol production after PMSG/hCG-induced ovulation.
Main Methods:
- Immature female rats were treated with PMSG and hCG to induce ovulation.
- Testosterone was administered to ovulated rats.
- Ovarian content of estradiol-17 beta was measured.
- Previous findings on ovarian enzyme activity (17 alpha-hydroxylase and C17-C20 lyase) were considered.
Main Results:
- Testosterone administration led to a significant increase in ovarian estradiol-17 beta content.
- This increase occurred despite a previously observed decrease in ovarian 17 alpha-hydroxylase and C17-C20 lyase activity post-PMSG/hCG treatment.
Conclusions:
- The post-ovulatory decrease in serum estradiol-17 beta is attributed to a limited supply of aromatizable androgens to ovarian aromatase.
- Diminished activity of ovarian 17 alpha-hydroxylase and C17-C20 lyase is the likely cause of this androgen shortage.
- Testosterone administration can overcome this limitation, supporting the role of androgen precursors in estradiol synthesis.