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Regulation of 17 beta-estradiol synthesis in the proestrous hamster: role of progesterone and luteinizing hormone

, : Regulation of 17 beta-estradiol synthesis in the proestrous hamster: role of progesterone and luteinizing hormone. Endocrinology 105(6): 1432-1439

In hamsters, after the LH [luteinizing hormone, lutropin] surge on proestrus, there is a shift in the pattern of ovarian steroidogenesis involving an abrupt decline in serum estrogen and testosterone (T) and a concomitant increase in serum progesterone (P). The roles of LH and P in controlling ovarian 17.beta.-estradiol (E2) production were examined using in vivo and in vitro methods. The administration of 10-200 .mu.g P at 1000 h on proestrus consistently depressed serum E2 within 1 h. The decline in serum E2 continued for the subsequent 3 h. Thereafter, serum E2 increased in response to the endogenous LH surge, since the rise in E2 could be prevented by phenobarbitol administration. The decline in serum E2 after exogenous P at 1000 h was not always associated with a decline in serum LH or FSH [follicle-stimulating hormone, follitropin]. Serum LH was the same in hamsters treated with 10 .mu.g P and in controls between 1100-1800 h. Serum FSH declined slightly but only during the 1st hour. The injection of 50 .mu.g P at 1000 h had no significant effect on serum androstenedione (A) and T levels. The injection of 17.alpha.-hydroxyprogesterone (17.alpha.-OHP), A or T had no effect on serum E2, indicating the specific effect of P in depressing serum E2. Simultaneous injection of T along with P was able to prevent the fall in E2 levels during the 1st hour only. Follicular estrogen synthesis in proestrous hamsters apparently is very sensitive to P and P may serve as an intraovarian regulator of estrogen synthesis. Contrary to the situation in vivo, the addition of P in vitro greatly enhanced E2 production (838 .+-. 27 pg/mg per h) during a 2-h incubation. The injection of 10 .mu.g LH (NIH-S-16) s.c. at 1000 h on proestrus significantly elevated serum E2 (267 .+-. 11 pg/ml) within 1 h, followed by a steady decline during the subsequent hours. By the end of the 5th hour, serum E2 was very much reduced (47 .+-. 6 pg/ml). Serum T increased significantly during the 1st hour (358 .+-. 28 pg/ml) and then declined steadily, paralleling the declining E2. P levels progressively increased (from 1-17 ng/ml serum) during the entire 5-h period. In the in vitro system, LH (250 ng/ml) stimulated E2 production during the entire 4-h incubation, since the production of E2 (as measured in the medium) was the same at the end of the first 2 h (2147 .+-. 257 pg/mg per ml) and at the end of the second 2 h (1745 .+-. 173 pg/mg per ml). In vitro, LH sustained E2 synthesis, whereas LH led to a rapid decline in serum E2 in vivo. The fall in serum E2 in normal hamsters begins at 1600 h on proestrus. Attempts were made to prevent this decline by administering P, 17.alpha.-OHP, A or T at 1300 h. The injection of 500 .mu.g T prevented the fall in serum E2, at least until 1800 h. A low dose of T (50 .mu.g) as well as 500 .mu.g P and 17.alpha.-OHP were unable to prevent the fall in E2, while A was partially effective. In the hamsters T is evidently a more readily aromatizable androgen. Higher T levels are probably needed for the maintenance of the aromatase system. These results apparently suggest a possible block in steroidogenesis at some point past 17-hydroxylation. The fact that the inhibitory effects of P were brought about much earlier than LH suggests that inhibitory effects of LH on E2 synthesis are most likely mediated through P. In the hamster LH evidently has a primarily stimulatory action on steroidogenesis, and its inhibitory effects on E2 synthesis are secondarily manifested through P or another factor(s) unknown at present.


PMID: 574076

DOI: 10.1210/endo-105-6-1432

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