The relationships among follicular growth, changes in serum progesterone (P) and estradiol (E) levels, and utero-ovarian blood flow (OBF) through the guinea pig ovary were examined during days 7-16 of the luteal phase (day 0 = estrus) of the estrous cycle and during the subsequent ovulatory (proestrous-estrous) period. Follicles were classified as either viable or atretic based on strict criteria and grouped according to diameter. No changes in follicular growth were observed between days 7-9 of the cycle when serum P levels were elevated and OBF was at low rates. Between days 13-15 when serum P levels were low and both OBF and serum E levels were rising, there was a dramatic increase in the number of viable follicles present in all follicle classes. As the percentage of viable follicles increased, the number of atretic follicles in each size population decreased. Peaks in the number of large follicles (300-450 microns), OBF, and serum E levels were observed during the subsequent ovulatory period. These data suggest that as luteal activity declines during the last half of the estrous cycle, follicular recruitment and growth are stimulated. The concomitant elevations in OBF suggest a supportive role for this parameter in follicular development. In turn, the subsequent elevation in serum E levels serves as an index of follicular maturation. These data suggest that the elevated P levels during the luteal phase of the estrous cycle may either directly or indirectly, through the regulation of gonadotropin secretion, regulate follicular growth in the guinea pig.
FSH in vitro stimulates increased oxygen uptake by isolated follicular granulosa cells from immature rats treated with diethylstilbestrol (DES) when substrates are present (glucose, glutamate, pyruvate or fumerate) or are completely absent. However, when glucose is the only substrate or when any single substrate is omitted from the buffer, FSH has no effect. FSH in vitro also increases the uptake of glucose and the formation of 14CO2 from [1-6 14C]-glucose. Granulosa cells from diabetic immature rats treated with DES did not show increased oxygen uptake with in vitro FSH. Diabetic cells had similar receptor binding of FSH to that of control non-diabetic cells. The addition of both insulin and FSH in vitro to buffer with diabetic granulosa cells gave increased oxygen uptake over that of control cells from diabetic rats. The insulin stimulation of oxygen uptake by FSH in cells from diabetic rats was not duplicated by either epidermal growth factor (EGF) or insulin-like growth factor I (IGF-1). Follicle counts of ovaries from diabetic and control immature rats treated with DES showed increased atresia in the diabetic ovaries after only 44 hr. of diabetes. Follicle counts of ovaries from adult diabetic rats showed increased atresia in 24 hours after induction of diabetes at proestrus. Follicle counts of pseudopregnant rats showed increased atresia by 3 days after diabetes was induced. We conclude that diabetes prevents normal follicle growth stimulated either by exogenous DES or by endogenous hormones secreted during proestrus.
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