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Biomedical subjects

W H Moger

Publications and source records attributed to W H Moger.

At least 55 records · Page 3Linked to original sources
PubMed1980

Studies on the interaction of 5 alpha-androstane-3 beta, 17 beta-diol with the testicular estrogen receptor.

5 alpha-Androstane-3 beta,17 beta-diol (3 beta-diol) was observed to inhibit [3H]estradiol ([3H]E2) binding to testicular cytosol preparations from both immature and mature rats with a potency of 1% that of diethylstilbestrol. The nature of the inhibition of [3H]E2 binding by 3 beta-diol was shown to be competitive with a KI of approximately 12 nM. This high competitive potency for a C19 steroid required both 3 beta- and 17-hydroxyl groups,, and reduced C5 position to inhibit E2 binding. Despite the interaction of 3 beta-diol with E2 receptor in vitro, injection of immature rats with 25 or 250 microgram 3 beta-diol 1-6 h before autopsy did not occupy or deplete the testicular cytoplasmic E2 receptor. When administered to immature female rats, 3 beta-diol did not show estrogenic agonistic or antagonistic activity in the uterus. These results suggest that the interaction of 3 beta-diol with the testicular receptor may be of little physiological significance.

Androstane-3,17-diol↗
PubMed1980

An unexpected increase in pituitary sensitivity to gonadotrophin releasing hormone after treatment with porcine follicular fluid (inhibin) in immature hemicastrate rats.

Porcine follicular fluid (PFF) contains a factor (inhibin or folliculostatin) which is reported to selectively inhibit the secretion of follicle-stimulating hormone (FSH) from the anterior pituitary gland. Chronic treatment of hemicastrate immature rats with PFF is able to partially inhibit the FSH-mediated hypertrophy of the remaining testis. However, the pituitaries from PFF-treated rats are paradoxically very sensitive to stimulation with gonadotrophin-releasing hormone (GnRH) and secrete significantly more FSH than control glands. Furthermore, this increased sensitivity results in a large increase in luteinizing hormone (LH) secretion. These observations suggest that under certain circumstances PFF is not selective for FSH and that it surprisingly stimulates rather than inhibits gonadotrophin secretion.

Animals↗
PubMed1980

Direct effects of estrogens on the endocrine function of the mammalian testis.

This article reviews literature relevant to the view that estradiol (E2) synthesized in the testis acts locally to modify testosterone secretion. Despite a lack of convincing evidence from in vitro experiments, in vivo experiments with intact and hypophysectomized animals have demonstrated that estrogens can inhibit testosterone secretion by acting directly on the testis. Reduced testosterone production in estrogen-treated animals probably results from reduced 17 alpha-hydroxylase and (or) C17-C20 lyase activity. Estrogen-inhibited steroidogenesis may result from estrogen binding to high affinity--low capacity estrogen receptors. Besides being an estrogen target tissue, the testis produces E2; the cellular site of testicular E2 synthesis remains controversial. Recent studies indicate that E2 is synthesized primarily in the Sertoli cells of neonatal rats and in the Leydig cells of older rats. Follicle-stimulating hormone and human chorionic gonadotropin (hCG) increase testicular aromatase activity and E2 concentrations in neonatal and older rats, respectively. An increase in testicular E2 concentrations, following hCG administration, may be one mechanism by which testosterone synthesis becomes desensitized to subsequent hCG stimulation. However, whether gonadotropin-stimulated testicular E2 synthesis is part of a physiologically relevant "short" feedback loop that participates in the regulation of testosterone synthesis remains to be determined.

Androgens↗
PubMed1979

Production of testosterone, 5 alpha-androstane-3 alpha, 17 beta-diol and androsterone by dispersed testicular interstitial cells and whole testes in vitro.

The production of 5 alpha-androstane-3 alpha, 17 beta-diol (androstanediol), androsterone and testosterone by whole rat testes and testicular interstitial cells dispersed with collagenase was studied in vitro. Luteinizing hormone stimulated the production of each of the androgens by cells prepared from 31- to 34-day-old rats. Half maximum stimulation of the production of each androgen occurred with approximately 3.5 ng NIH-LH-B9/ml medium. Androstanediol was the predominant product then androsterone and then testosterone. Luteinizing hormone stimulated the production of testerone, but not androstanediol or androsterone by dispersed interstitial cells from 200-day-old rats. The time-course of production and the effect of the concentration of cells on the production of these androgens suggested that in dispersed testicular interstitial cells from immature animals androstanediol and androsterone are formed, at least partially, by the metabolism of testosterone. In these experiments LH-stimulated testosterone production increased during incubation for 15--60 min and then remained constant up to 180 min. The concentrations of androstanediol and androsterone increased in a linear manner during incubation for 60--180 min. Varying the number of cells incubated yielded a positive correlation between cell concentration and the ratio 5 alpha-reduced androgen : testosterone produced. Luteinizing hormone stimulated production of each androgen by whole tests obtained from rats at 30--175 days of age. The serum concentration of testosterone in these rats increased abruptly at 50 days of age. Significant changes in androgen production in vitro also observed at this age included: (1) increased production of the three steroids when incubated in either the presence or absence of LH and (2) testosterone production, either in the presence or absence of LH, which represented a greater percentage of the total production of the three androgens.

Age Factors↗
PubMed1977

Radioimmunoassays for androsterone, 5alpha-androstane-3alpha, 17beta-diol and 5alpha-androstane-3beta, 17beta-diol.

Androsterone (3alpha-hydroxy-5alpha-androstan-17-one), 5alpha-androstane-3alpha, 17beta-diol and 5alpha-androstane-3beta, 17beta-diol were conjugated at C-16 through sulfur to bovine and human serum albumin. Rabbits injected with these conjugates produced antibodies suitable for radioimmunoassays of these hormone metabolites. Samples were purified on Sephadex LH-20 columns. Levels of these steroids were measured in a rat blood serum pool and in ovarian tissue extract pools.

Androstane-3,17-diol↗
PubMed1977

Progestins of mink gestation: the effects of hypophysectomy.

Progesterone and 20alpha-hydroxypregn-4-ene-3-one (20alpha-ol) were determined from plasma samples taken weekly beginning 10 - 18 days before implantation in Pearl variety mink. Progesterone was low ( less than 8 ng/ml) until approximately five days prior to implantation when it increased and remained elevated (congruent to 30 ng/ml) through the early portion of postimplantation pregnancy. A subsequent decline was observed toward parturition. Mean concentrations of 20alpha-ol were relatively constant through gestation with a trend toward a greater proportion of progestin represented as 20alpha-ol during the preimplantation delay. Hypophysectomy prevented implantation, reduced progesterone levels and increased the concentration of 20alpha-ol relative to progesterone in plasma. These data suggest that prolactin (PRL) is a component of the luteotrophic complex in mink. Further, the corpus luteum of delay requires hypophyseal support for normal function.

20-alpha-Dihydroprogesterone↗
PubMed1977

The effect of FSH on LH induced testosterone secretion in the immature hypophysectomized male rat.

The effect of gonadotropin pretreatment of hypophysectomized male rats on LH stimulated serum testosterone concentrations was studied. A 5 day pretreatment period began 2 days after hypophysectomy at 21 or 24 days of age. On the day following the pretreatment period the animals received an intraperitoneal injection of saline or LH 60 min before blood collection. Animals pretreated with NIH-FSH-B1, or with doses of LH approximating the amount present in the NIH-FSH, had increased testosterone concentrations after LH stimulation compared to similarly stimulated saline pretreated animals. Pretreatment with more highly purified FSH Ex 199C at a lower dose than the minimum effective dose of NIH-FSH was also effective. There was no synergistic or additive effect when FSH Ex 199C and LH pretreatments were combined. FSH Ex 199C is more potent and contains appreciably less LH contamination than NIH-FSH-B1. The results obtained using FSH Ex 199C indicate that FSH, independent of LH contamination, can increase testes response to LH stimulation.

Animals↗
PubMed1977

Modulation of pituitary responsiveness to LHRH by androgens in ovariectomized female rats.

The effect of androgens on pituitary response to luteinizing-hormore-releasing hormone (LHRH) and their ability to modify effects of 17beta-estradiol (E2) on pituitary responsiveness to LHRH were tested in ovariectomized rats maintained on a daily dose of 0.25 microgram estradiol benzoate per rat for 6 d before androgen administration. Testosterone propionate (TP) (4, 40, 400, or 4000 microgram per rat), administered 24 h before LHRH (500 ng per rat), had no significant effect on luteinizing hormone (LH) or follicle-stimulating hormone (FSH) response. Similar doses of dihydrotestosterone (DHT) did not significantly alter the LH response but significantly suppressed the FSH response. Even the lowest dose completely blocked the FSH response to LHRH. TP in combination with 4 or 400 microgram of E2 suppressed the stimulatory effect of E2 on both LH and FSH response to LHRH in a dose-related manner. DHT and E2 in combination affected LH response inconsistently, whereas their ratio determined FSH response; there was pronounced inhibition of FSH response in rats given high doses of DHT combined with low doses of E2; DHT inhibition of FSH response in animals receiving 4 microgram of DHT with 400 microgram E2 was partially overcome by the stimulatory effect of E2. Our results indicate that TP and DHT affect LH and FSH response to LHRH differently. The ratio of androgen to estrogen is important in determining the response to LHRH.

Androgens↗
PubMed1977

Serum 5alpha-androstane-3alpha,17beta-diol, androsterone, and testosterone concentrations in the male rat. Influence of age and gonadotropin stimulation.

Serum concentrations of testosterone plus dihydrotestosterone (T-DHT), 5 alpha-androstane-3 alpha, 17 beta-diol (Diol) and androsterone were measured during sexual maturation in male rats. Diol concentrations of 1 to 2.25 ng/ml were found in animals 10-90 days of age with no significant changes. Diol was the major androgen (5.75-8 times T-DHT) from age 20-40 days. Androsterone rose to 1.25 ng/ml at 25 days of age and declined to values of greater than 0.5 ng/ml from age 30-90 days. Testosterone-DHT levels were 1 ng/ml or less from 10-40 days of age, and then rose to a peak at 60 days. The ratio of Diol toT-DHT was significantly elevated from age 20-35 days, indicating that Diol is the major androgen in circulation at this time. Acute treatment of 33 day old rats with LH, but not with FSH, resulted in a dose-dependent increase in serum T-DHT, Diol, and androsterone. The dose-response and time course of response for the three steriods were nearly identical. Changes in testes capacity to secrete androgens were assessed 25, 33, 40 and 60 days of age by administering a maximum dose of LH before blood collection. Maximum response (sum of androsterone, Diol and T-DHT) occurred at 40 days with no further increase at 60 days.

Aging↗