Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “testosterone secretion”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,729 records · Page 96Linked to original sources
PubMed1989

Regulation of steroidogenesis in cultured porcine theca cells by growth factors.

Growth factors [insulin-like growth factors (IGF-I, IGF-II), transforming growth factor-beta (TGF beta), epidermal growth factors (EGF)], found in the ovary and known to alter granulosal function, were assessed for their ability to modulate porcine thecal steroidogenesis. Theca cells from large porcine follicles (8-10 mm) were plated (5 x 10(5) cells/ml.well) in serum-free M199, treated with increasing doses of growth factors: IGF-1 (0.1-50 ng/ml), IGF-II (0.5-200 ng/ml), EGF (0.021-100 ng/ml), TGF beta (0.001-40 ng/ml), or insulin (0.01-50 micrograms/ml), with or without human CG [(hCG); 20 ng/ml], and incubated for 72 h. Levels of steroids in media were determined by RIA. Insulin increased (P less than 0.05) basal and gonadotropin-induced secretion of androstenedione, progesterone, estradiol, and testosterone. IGF-I increased (P less than 0.05) the basal and hCG-induced secretion of progesterone and androstenedione at the highest doses, but did not affect basal secretion of estradiol or testosterone. IGF-II, at the highest doses, increased (P less than 0.05) thecal steroidogenesis, but only after administration of hCG. In contrast, TGF beta increased (P less than 0.05) basal and gonadotrophin-induced secretion of estradiol but inhibited thecal secretion of progesterone, androstenedione, and testosterone. EGF did not alter thecal secretion of progesterone, androstenedione, or testosterone but significantly (P less than 0.05) inhibited basal and hCG-stimulated secretion of estradiol. In conclusion, insulin IGF-I, IGF-II, EGF, and TGF beta can modulate steroidogenesis in porcine theca cells.

Animals↗
PubMed1990

Effects of androgen on progesterone secretion from granulosa cells obtained from antral follicles of rats.

The effects of testosterone (T) on the secretion of progesterone (P) by ovarian granulosa cells obtained from immature rats pre-treated with pregnant mare's serum gonadotropin were examined in vitro. T (10 nM-10 microM) enhanced both basal and FSH- or cAMP-stimulated secretion of P in a dose-dependent manner. Furthermore, T augmented FSH-stimulated cAMP production. The biphasic secretory pattern of P induced by continuous superfusion of granulosa cells with FSH was much exaggerated in the cultures supplemented with T. A stimulatory effect of T on secretion of P was observed only in the medium that contained serum. T affected neither the basal nor the FSH-stimulated secretion on 20 alpha-dihydroprogesterone. Androsterone, a non-aromatizable and low-potency androgen, at a similar concentration as T mimicked the effects of T on the secretion of progesterone. These results indicate that androgen stimulates mature granulosa cells to enhance the secretion of P. This androgen action extends either up- or down-stream of cAMP in the process of steroidogenesis.

20-alpha-Dihydroprogesterone↗
PubMed2001

Fertility and sexual life of men after their forties and in older age.

Owing to the demographic development, the aging male will require more consideration in future. In contrast to a rapid decline of estradiol during menopause in women, the process of aging in the male is retarded and subject to high individual variations. Impairment of spermatogenesis is observed as a continuous process occurring over decades. However, only about 50 % of men in their eighties show complete loss of fertility. In principle, spermatogenesis may be retained well into senescence. Of importance for the individual health condition is the fact that the number of Leydig cells declines with advancing age. Thus, altered sex hormone concentrations in aging men result from both functional disturbances and a gradual reduction in Leydig cells. Furthermore, an impaired feed-back mechanism of the pituitary-gonadal axis occurs, with disappearance of the circadian testosterone (T) rhythm. LH and FSH levels are increased, and a reduced bioavailability of sex hormones is observed. Lower total testosterone concentrations in men over 60 years are accompanied by clinical signs of reduced virility, such as decreased muscle mass and strength as well as reduced sexual hair growth and libido. An age-related decline in androgen secretion and plasma testosterone levels therefore suggests the use of androgen supplementation. However, there is a lack of risk-benefit long-term studies. Increased research in the male is mandatory to meet the requirements of the aging population. This should include the availability of precise epidemiological data about the frequency of partial androgen deficiency in aging males (PADAM).

Adult↗
PubMed1988

[Release of steroid hormones in vitro by ovarian follicles of various degrees of maturity in hens and cows].

The growth of ovary follicules was accompanied by a considerable decrease in the secretion of progesterone, testosterone and estradiol, as well as by a decrease of the estradiol share in total hormone production,--both in hens and in cows. The hens also revealed a decrease of the testosterone share and an increase of the progesterone share in total hormone production. the data obtained suggest a functional atresia of the ovary follicules in hens as well as in mammals. the hen mature follicules, however, differ from those of mammals in that the progesterone secretion is higher in them as compared with other steroids, the progesterone being the main ovulatory hormone in birds.

Animals↗
PubMed2006

Age or factors associated with aging attenuate testosterone's concentration-dependent enhancement of the regularity of luteinizing hormone secretion in healthy men.

BACKGROUND: Healthy older men have reduced testosterone (Te) production and frequent, small irregular LH pulses. Which is cause and which is effect are not known. RATIONALE: In model systems, frequent and irregular LH pulses reflect attenuated feedback inhibition by Te. HYPOTHESIS: Factors associated with aging impair negative feedback by Te. SUBJECTS AND SETTING: Healthy men at an academic medical center were studied. METHODS: The study used quantification of the regularity of LH release patterns during blockade of gonadal steroidogenesis and graded transdermal Te addback in 18 healthy men aged 18-65 yr. RESULTS: In the cohort as a whole, stepwise Te repletion repressed LH concentrations (P = 0.001) and enhanced the quantifiable orderliness of LH release patterns (P < 0.001). By regression analysis, age attenuated the capability of increasing Te concentrations to regularize LH secretion patterns (P = 0.019). However, after a fixed GnRH stimulus, the effect of Te on LH regularity was invariant of the age factor (P = 0.16), thus pointing to a hypothalamic locus of impaired Te feedback. SUMMARY: Aging disrupts the capability of systemic Te concentrations to maintain orderly LH secretion under endogenous, but not exogenous, GnRH drive. CONCLUSIONS: Age or factors associated with increased age reduce negative feedback by any given total Te concentration on hypothalamopituitary GnRH-LH outflow, thus contributing to disorderly LH secretion.

Adult↗
PubMed1979

Effects of estrogens on the testosterone levels of peripheral and spermatic vein blood in patients with prostatic cancer.

The mean testosterone levels of peripheral and spermatic vein blood in 16 patients with prostatic cancer who did not have estrogen therapy were 418.2 plus or minus 30.8 ng./dl. (mean plus or minus standard error) and 39.7 plus or minus 5.6 micrograms/dl., respectively. There were 13 patients with prostatic cancer who received estrogen therapy with daily doses of 30 mg. hexesterol or 300 mg. diethylstilbestrol diphosphate and who had decisive decreases of testosterone levels in peripheral (90.1 plus or minus 23.2 ng./dl.) and spermatic vein blood (3.3 plus or minus 1.2 migrogram/dl.). The rate of reduction of testosterone by estrogen therapy was one-tenth in the spermatic vein blood, while that in the peripheral blood was one-fifth. These data indicate that continuation of oral estrogens of these doses is sufficient to suppress the testicular androgens. On the other hand, the spermatic testosterone concentration was about 40 times higher than the peripheral testosterone concentration in patients receiving estrogen treatment. This result suggests that testosterone still is secreted from the testes under large therapeutic doses of estrogens.

Adult↗
PubMedDate not supplied

Effects of single non-ortho, mono-ortho, and di-ortho chlorinated biphenyls on cell functions and proliferation of the human prostatic carcinoma cell line, LNCaP.

This study investigated the effects of the non-ortho 3,3',4,4',5-pentachlorobiphenyl (PCB 126) and 3,3',4,4'-tetrachlorobiphenyl (PCB 77), the mono-ortho 2,3',4,4',5-pentachlorobiphenyl (PCB 118), and the di-ortho substituted 2,2',4,4',5,5'-hexachlorobiphenyl (PCB 153) on the human prostatic carcinoma cell line LNCaP. Activities of 5alpha-reductase and ethoxyresorufin-O-deethylase (EROD) secretion of testosterone-regulated prostatic specific antigen (PSA) and cell proliferation served as specific and general cell markers. The two non-ortho (dioxin-like) PCBs, PCB 126 and PCB 77, showed anti-androgenic properties. Both PCBs reduced androgen-depending PSA secretion and cell proliferation, and inhibited the DHT-producing enzyme 5alpha-reductase in a concentration-dependent manner. In contrast, the ortho-substituted PCBs, PCB 118 and PCB 153, had no effect on 5alpha-reductase. However, they had a biphasic effect on LNCaP cell proliferation. PCB 153 and, to some extent, PCB 118 induced cell proliferation and PSA secretion at low concentrations, whereas, these parameters were reduced at high concentrations. Since EROD induction and inhibition of 5alpha-reductase activity was not observed, these findings suggest an AhR and AR independent mechanism and post-transcriptional target sites should be considered. The effects of PCB 126 on cell proliferation, PSA secretion, and 5alpha-reductase activity may be partly a result of AhR-dependent inhibition. In conclusion, the endocrine activity of PCBs via direct steroid hormone receptor-mediated and Ah receptor-mediated pathways are well known. However, the modulation of post-transcriptional targets may account for some of the endocrine disrupting properties of single PCB congeners.

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗
PubMed2001

Antagonism of central vasopressin receptors blocks hypoglycemic stress induced inhibition of luteinizing hormone release in male rhesus macaques.

The first objective of this study was to investigate whether the inhibitory effect of insulin-induced hypoglycemia (IIH) on luteinizing hormone (LH) secretion was the same in unrestrained adult male rhesus macaques as has been previously reported in restrained female macaques. Since IIH did inhibit pulsatile LH secretion in adult male macaques, and some previous studies have implicated arginine vasopressin (AVP) as a central mediator of this inhibition, the second objective was to investigate whether antagonism of AVP action could reverse the IIH-induced inhibition of LH release in males. Ten adult male rhesus macaques (Macaca mulatta) were studied during 15-h periods (07.00-22.00 h), with blood samples collected every 15-min. There were three experimental groups; controls (n = 5), IIH (n = 6) and IIH plus vasopressin antagonist (AVPa; n = 6). During the hypoglycemia studies, the first 5 h served as a control for that occasion and an insulin bolus of 1 U/kg was administered intravenously at 12.00 h. During the IIH plus AVPa, the vasopressin antagonist was infused intravenously from 12.00 h to 17.00 h. LH and testosterone decreased progressively after the insulin bolus in the IIH group reaching a minimum value at 4 h after the infusion. However, compared to the preinfusion levels, secretion of LH and testosterone was not suppressed by hypoglycemia in the group treated with the AVP antagonist. The present study shows that in male macaques not subjected to the psychological stress of restraint, IIH suppresses LH and testosterone secretion. This inhibition of LH release can be blocked in some animals by antagonism of central vasopressin receptors, suggesting that vasopressin is involved in the suppression of gonadotropin releasing hormone/LH release induced by hypoglycemia.

Animals↗
PubMed1979

Regeneration of atretic sheep ovarian follicles in vitro.

Large (4--6 mm diam.) and small (2--3 mm) atretic follicles were removed from sheep ovaries during the luteal phase of the cycle and maintained in organ culture without hormonal supplementation for up to 5 days. The structure, cell dynamics and steroid-producing capacity of the follicles were compared with those of non-atretic follicles of similar size. The granulosa layer of the atretic follicles invariably regenerated in culture, increasing in thickness more than 2- and 4-fold in large and small follicles respectively. This could not be accounted for by cell division which remained low throughout the culture period. In contrast, non-atretic follicles showed high mitotic activity during the first 24 h in culture: this was not associated with an increase in granulosa thickness in large follicles although there was a 4-fold increase in small ones. An increase in internuclear spacing, a measure of cell size plus intercellular space, partly accounted for the increase in granulosa thickness in atretic follicles. Even when granulosa cells remained in close apposition there was an almost total absence of gap junctions, a prominent feature in the granulosa of non-atretic follicles both in vivo and in vitro. Pyknotic nuclei and atretic bodies rapidly disappeared from the regenerating granulosa layer. The theca interna was restored in culture to a state ultrastructurally closely resembling that of non-atretic follicles in vivo. Total steroid secretion (oestradiol-17beta, testosterone plus progesterone) into the culture medium (pmol.mg tissue-1.24 h-1) was the same for atretic and non-atretic follicles of comparable size. There was, however, a marked difference in the type of steroid produced, largely related to a loss of aromatizing capacity in atretic follicles. The predominant steroid secreted by large non-atretic follicles was oestrogen, with slightly smaller amounts of testosterone, whereas the principal steroid secreted by large atretic follicles was progesterone. In small non-atretic and atretic follicles, the predominant steroid was testosterone, but the non-atretic follicles also secreted appreciable amounts of oestrogen. Addition of FSH to the culture medium did not restore aromatizing capacity to the atretic follicles.

Animals↗
PubMed1993

Salivary testosterone in children with and without learning disabilities.

Previous studies have indicated that the sex steroids have organizational effects upon neural tissue and that abnormal secretion during development may lead to functional anomalies. In this study, we explore the possibility of prepubertal steroid hormone involvement in the etiology of learning disabilities. Salivary testosterone levels in 264 children without learning disabilities (133 males, 131 females) were measured and compared to that in 32 children with learning disabilities (25 males, 7 females). The presence of learning disabilities was significantly associated with higher salivary testosterone. Data from equivalent samples of learning-disabled and control subjects also were compared separately because of disparities in sample size and variable distribution in the total group analysis. A 32-member sample of nonlearning-disabled children was created by randomly selecting individuals who exactly matched the age, race, and sex characteristics of the learning-disabled group. The matched analysis further substantiated the association between testosterone secretion and learning disabilities. Thus, it is possible that some learning disabilities may be associated in part with abnormal testosterone levels.

Adolescent↗
PubMed1983

Aromatization: important for testosterone's developmental influences on the neurocircuits mediating cervically stimulated prolactin secretion in the female rat.

Adult female rats treated neonatally with testosterone or estrogen fail to respond to cervical stimulation with episodic prolactin release. The developmental action of testosterone is inhibited by co-administration of 1,4,6-androstatriene-3,17-dione at a dose sufficient to inhibit the testosterone-induced rise in estrogen receptors in limbic brain cell nuclei. These data suggest the importance of aromatization for testosterone action.

Animals↗
PubMedDate not supplied

Feminizing adrenocortical adenoma presenting as heterosexual precocious puberty: report of one case.

We report on a case of a 2 2/12-year-old boy with heterosexual precocious puberty secondary to a feminizing adrenocortical adenoma. The boy, with no previous history of disease or treatment, presented with bilateral gynecomastia and pubic hair development (Tanner III breasts and Tanner II pubic hair). Plasma estradiol and testosterone were 410.9 pg/ml and 126.2 ng/dl respectively. Basal plasma LH and FSH levels were within the normal range. Bolus i.v. injection of GnRH showed unresponsiveness of LH and FSH. Abdominal echography and abdominal magnetic resonance imaging revealed a well-defined mass at the left suprarenal region (measuring 4.0 x 2.7 x 3.6 cm in size). After removal of the adrenal tumor, the estradiol and testosterone levels fell to normal in 2 weeks. The gynecomastia and pubic hair regressed with time. The pathology of the tumor showed compact pattern with polygonal cells containing moderate eosinophilic cytoplasm without mitotic figure. These findings were consistent with an adrenocortical adenoma secreting estradiol and testosterone as the cause of the patient's heterosexual precocious puberty.

Abdomen↗
PubMed1992

The in vitro perifused rat ovary: I. Steroid secretion in response to ramp and pulsatile stimulation with luteinizing hormone and follicle stimulating hormone.

A computer-controlled perifusion apparatus has been used to investigate the effects of different patterns of hormonal stimulation on secretion of steroids by ovaries from untreated, or pregnant mare serum gonadotropin (PMSG)-pretreated, immature rats. With ovaries from untreated rats, a low rate of increasing concentration of gonadotropins (luteinizing hormone (LH) plus follicle stimulating hormone (FSH)) induced a maximum secretion of estradiol within 60 min (22.6 +/- 1.4 pg/mg/30 min). An intermediate and a high rate of increasing gonadotropin concentration stimulated maximum secretion (26.0 +/- 1.2 pg/mg/30 min) and 28.1 +/- 2.8 pg/mg/30 min), respectively) within 30 min. Peak secretion, however, was not maintained and was reduced despite continued LH/FSH pulses. Progesterone secretion increased during, and subsequent to, the decreasing estradiol output. Increasing amplitudes of LH/FSH or constant perifusion with LH/FSH did not change the profile, or the concentration of estradiol, but these measures increased progesterone release. An occasional transient increase in estradiol secretion was observed when ovaries from unstimulated rats were perifused with low LH/FSH pulse frequency. Thus, these studies support the hypothesis that in the prepubertal rat ovary, elements of pulse characteristics, such as rate of increasing LH/FSH concentration, and amplitude are important in differentially regulating steroid output. The steroid secretory pattern of ovaries from PMSG-treated prepubertal rats was different from that of untreated rats. With ovaries from PMSG-treated rats, an acute increase in secretion of progesterone, testosterone or estradiol was not observed, whether low or high rates of increasing gonadotropin concentration were used. Rather, the concentration of these steroids continued to rise following LH/FSH pulses. Thus, in contrast to the untreated ovary, the PMSG-treated ovary did not show differential regulation of steroid secretion in response to LH/FSH. In conclusion, we have shown the in vitro perifusion model to be a useful tool for studying the effects of different patterns of hormonal stimulation on ovarian steroidogenesis. In addition, differential effects of gonadotropins on steroid output were shown, depending upon prior maturation of the ovary.

Animals↗
PubMed1980

Alteration in the normal pattern of serum testosterone and 5 alpha-androstane-3 alpha, 17 beta-diol in the immature male rat following chronic treatment with luteinizing hormone releasing hormone or luteinizing hormone.

A major component of sexual maturation in the male rat is a progressive decline in serum concentrations of 5 alpha-androstane-3 alpha, 17 beta-diol (3 alpha-diol) and a concomitant increase in testicular testosterone biosynthesis and secretion. Chronic administration of synthetic luteinizing hormone releasing hormone (LHRH) or luteinizing hormone (LH)/human chorionic gonadotropin (hCG) to immature male rats has been shown to result in a delay in sexual maturation as evidenced by decreased sex accessory gland weights and altered testicular testosterone production. We have examined the postulate that such treatments may either reverse or retard the normal developmental pattern of serum testosterone and 3 alpha-diol concentrations. Chronic in vivo treatment of 28 day old immature male rats for 2 weeks with daily injections of either 0.5 micrograms of LHRH, 1.0 micrograms of LHRH, or 30 micrograms of LH was found to result in significant reductions in weights of the seminal vesicles and ventral prostate glands and diminutions in serum testosterone concentrations. Serum content of 3 alpha-diol was either unchanged or slightly elevated in the LHRH treated animals and increased significantly in the LH treated animals. These data suggest that either a reversal of or retardation in the normal developmental pattern of serum testosterone and 3 alpha-diol content has been achieved in the immature male rat by chronic LHRH or LH treatment.

Androstane-3,17-diol↗
PubMed1988

Divergent effects of the antiestrogen tamoxifen and of estrogens on luteinizing hormone (LH) pulse frequency, but not on basal LH levels and LH pulse amplitude in men.

We studied the role of estrogens on LH pulse modulation in men in two ways. Firstly, we compared LH pulse frequency and amplitude in 13 normal men before and after 6 weeks administration of the antiestrogen tamoxifen (10 mg twice daily). Secondly, we compared LH pulse frequency and amplitude between a group of 10 agonadal men not receiving sex steroid treatment and a group of 9 agonadal men (male to female transsexuals) continuously treated with 50 micrograms ethinyl estradiol/day. Tamoxifen administration to normal men resulted in a significant rise in the mean serum LH level from 5.7 +/- 1.3 (+/- SD) to 10.1 +/- 2.4 U/L, which was associated with significant increases in LH pulse frequency (from 4.2 +/- 1.5 to 5.8 +/- 1.7/7 h) and LH pulse amplitude (from 3.8 +/- 0.9 to 4.6 +/- 0.7 U/L). In the group of agonadal men the mean LH pulse frequency was 6.8 +/- 1.5/7 h, while it was 5.9 +/- 1.7/7 h in the estrogen-treated agonadal group (P = NS). The mean serum LH level and LH pulse amplitude were, however, significantly lower in the estrogen-treated agonadal men than in the agonadal men (14.7 +/- 7.0 vs. 34.3 +/- 8.6 and 4.1 +/- 1.8 vs. 7.4 +/- 1.8 U/L, respectively). We conclude that estrogens reduce basal LH levels and LH pulse amplitude. With regard to the modulation of LH pulse frequency our data provide contradictory results. While an antiestrogen increased LH pulse frequency in normal men, estrogen alone produced no change in LH pulse frequency in agonadal men. The study design in the agonadal men ignores the possible interaction of the two major testicular hormones (estradiol and testosterone) on gonadotropin secretion. Therefore, a possible explanation for this discrepancy in the effects of antiestrogen and estrogen could be an interaction between estrogens and androgens on gonadotropin secretion at the level of the LHRH pulse generator.

Adult↗