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 469 records · Page 26Linked to original sources
PubMed2006

Duration of testosterone suppression after a 9.45 mg implant of the GnRH-analogue buserelin in patients with localised carcinoma of the prostate a 12-month follow-up study.

OBJECTIVES: (1) To determine the duration of androgen deprivation after a single buserelin implant 9.45 mg in the neoadjuvant setting in combination with curative radiation therapy of carcinoma of the prostate, and (2) to evaluate the time to recovery of gonadal function, and the incidence and duration of hypogonadal symptoms. METHODS: We prospectively evaluated 21 men with carcinoma of the prostate who received one implant of 9.45 mg buserelin subcutaneously. Release of buserelin, changes in serum testosterone concentration, hot flushing and sexual function over a 12-month study period were recorded. RESULTS: Testosterone was suppressed below the castration limit (0.58 ng/ml=2 nmol/l) for 224 days (range, 139-309). The mean time to first return of testosterone above the castration limit was 246 days (range, 168-344); 50% of pre-treatment value was reached after 285 days (range, 218-370). The prevalence of hot flushing was 19 of 21 patients (90%) at 12 weeks. At the end of the study period, serum testosterone had reached 80% (range, 33%-166%) of pre-treatment concentration, sexual interest was present in 52%, erection was possible in 60%, and hot flushing remained in 24%. CONCLUSION: A single injection of 3-month buserelin implant 9.45 mg suppresses serum testosterone below the castration limit for at least 6 months. Testosterone secretion recovers by 8-12 months. Hypogonadal symptoms decreased with the restoration of serum testosterone secretion. These data are clinically relevant regarding the dose schedule for buserelin and the patient information provided.

Aged↗
PubMed1985

Regulation of testosterone production in Leydig cells from fetal mice under dynamic conditions: effect of human chorionic gonadotrophin and 8-bromo-cyclic AMP.

The temporal release of testosterone by Leydig cells from 18-day-old mouse fetuses in response to human chorionic gonadotrophin (hCG) and to 8-bromocyclic AMP (8-bromo-cAMP) was investigated under short-term incubation (180 min) conditions. A rapid and large increase in testosterone release was induced by a 5-min exposure to hCG (20 i.u./l) or 8-bromo-cAMP (10 mmol/l). The testosterone response of fetal Leydig cells to the two gonadotrophic stimuli was Gaussian in distribution with a peak value of testosterone by 15-20 min. Repeated exposure to hCG resulted in a reduced testosterone response but an increased accumulation of cAMP. The apparent resistance of fetal Leydig cells to hCG could not be overcome either by increasing the hCG concentration (to 2000 i.u./l) or by exposing the cells to 8-bromo-cAMP (10 mmol/l). Continuous exposure to hCG (200 i.u./l) divided into multiple small doses (each 8 i.u./l) induced testosterone secretion with different kinetic characteristics: a three-fold longer time-lag between hormone exposure and the peak value; a twofold greater testosterone response (P less than 0.001) and a gradual decrease of testosterone secretion. Oestradiol significantly reduced basal and hCG-stimulated testosterone production only at a high concentration (10 mumol/l). These results indicate that continuous or pulsatile exposure to hCG can induce refractoriness of fetal Leydig cells. The similarity between the actions of hCG and 8-bromo-cAMP on fetal steroidogenesis suggests that this rapid defect is not primarily due to a depletion of gonadotrophin receptors but results from disruption of regulatory mechanisms at the post-receptor level.

8-Bromo Cyclic Adenosine Monophosphate↗
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↗
PubMed1984

A comparison of corticoadrenal and gonadal responses to acute immobilization stress in rats and mice.

The effect of different periods of acute immobilization stress on circulating corticosterone and testosterone was studied in adult male rats and mice. Although initial corticoadrenal response to immobilization was similar in both species, this differed after a more prolonged exposure to the stress stimulus. This suggests that behavioral adaptation to long-lasting stimulation and/or effectiveness of corticosterone feedback on the hypothalamus-pituitary-adrenal axis could be different in those species. An inhibition of testosterone secretion after 5 hr of immobilization was observed in both rats and mice. However, mice seem to be more sensitive to stress-induced inhibition of testosterone secretion than rats. No evidence for a biphasic testosterone response to stress was found.

Adrenal Cortex↗
PubMed2002

Decreased pituitary-gonadal secretion in men with obstructive sleep apnea.

Decreased libido is frequently reported in male patients with obstructive sleep apnea (OSA). The decline in morning serum testosterone levels previously reported in these patients was within the normal adult male range and does not explain the frequent association of OSA and sexual dysfunction. We determined serum LH and testosterone levels every 20 min between 2200-0700 h with simultaneous sleep recordings in 10 men with sleep apnea and in 5 normal men free of any breathing disorder in sleep. The mean levels and area under the curve of LH and testosterone were significantly lower in OSA patients compared with controls [LH, 24.9 +/- 10.2 IU/liter.h vs. 43.4 +/- 9.5 (P < 0.005); testosterone, 67.2 +/- 11.5 nmol/liter.h vs. 113.3 +/- 26.8 (P < 0.003)]. Four of 10 patients had hypogonadal morning (0700 h) serum testosterone levels. Analysis of covariance (ANCOVA) revealed that the 2 groups differed significantly in the amount of LH and testosterone secreted at night independent of age or degree of obesity. After partialing out body mass index, there was a significant negative correlation between the amounts of LH and testosterone secreted at night and the respiratory distress index, but not with degree of hypoxia. Our findings suggest that OSA in men is associated with dysfunction of the pituitary-gonadal axis. The relation between LH-testosterone profiles and the severity of OSA suggests that sleep fragmentation and, to a lesser extent, hypoxia in addition to the degree of obesity and aging may be responsible for the central suppression of testosterone in these patients.

Adult↗
PubMed2003

Luteinizing hormone beta polymorphism and risk of familial and sporadic prostate cancer.

BACKGROUND: Circulating testosterone plays an important role in maintenance and growth of prostate cells. Luteinizing hormone (LH), secreted from the anterior pituitary, signals testicular Leydig cells to secrete testosterone. A genetic variant of the LH-beta protein, LH-betaV, exists in up to 40% of Caucasians and is more bioactive than the wild-type protein. We hypothesized that genetically determined variation in LH function might affect susceptibility to prostate cancer via altered testosterone secretion. METHODS: We determined the frequency of the LH-betaV polymorphism (two linked polymorphisms: Trp(8) --> Arg and Ile(15) --> Thr) in familial prostate cancer patients (n = 446), in sporadic prostate cancer patients (n = 388), and in population-based controls without prostate cancer (n = 510) to assess the role of this polymorphism in susceptibility to prostate cancer. RESULTS: A higher frequency of this variant genotype (LH-betaV: Arg(8)/Thr(15)) was observed in familial prostate cancer patients (18.6%) than in controls (13.7%), and after taking into account the correlation of the familial cases and adjusting for age and body mass index (BMI), there was a weak positive association between the variant LH-beta genotype, and risk of familial prostate cancer (OR = 1.29; 95% CI 0.96-1.75). The sporadic case group was also slightly more likely to have a variant genotype (15.2%) compared to the controls (13.7%), and after adjustment for age and BMI, a similar association with this variant was found (OR = 1.33; 95% CI 0.86-02.07). Surgical cases showed a slightly stronger association for the variant LH-beta genotype compared to non-surgical cases, but among the surgical cases there was little variability in risk across nodal status, stage, and tumor grade. CONCLUSIONS: These data are consistent with the hypothesis that the LH-beta variant is a weak risk factor for prostate cancer.

Adult↗
PubMed1997

Improvement of cytochrome P450c17 catalytic processivity as a novel mechanism to attenuate hormonal consequences of enzyme decay in the testes after a gonadotropin surge.

OBJECTIVE: The aim of this study was to gain understanding of the apparent discrepancy between the moderate restriction of testosterone synthesizing capacity and the nearly complete decay of the androgen-producing enzyme, cytochrome P450c17 (CYP17; steroid 17 alpha-hydroxylase/17,20-lyase), in rat testes during the desensitization phase induced by a single, high-dose gonadotropin (human chorionic gonadotropin, hCG) injection. DESIGN AND METHODS: Adult male rats received 25 IU hCG i.v., and purified Leydig cells and crude interstitial cell microsomes were prepared 0, 4, 12, 24, 48, 72, 120 and 192 h afterwards. Component CYP17 activities, i.e. simultaneously catalyzed productive androgen formation and abortive 17 alpha-hydroxyprogesterone release, and their ratio (processivity), were compared with CYP17 levels and testosterone secretion rates. RESULTS: Leydig cells isolated 48 h after the artificial hCG surge produce 62% less testosterone than control cells upon stimulation in vitro, though CYP17 levels are reduced by 97%. Its total activity decreases by 87%, resulting in a 4.5-fold rise in the turnover number; the processivity is additionally improved 5-fold over controls. Parallel changes occur in interstitial cell microsomes; a negative linear correlation exists between the ratio of productive over total CYP17 activities and the actual CYP17 concentrations. CYP17 is partly denatured to P420 during hCG action, but other heme proteins (cytochrome b5) remain unchanged. Animal treatment with estradiol results in CYP17 down-regulation without any concomitant effect on enzyme processivity. CONCLUSION: Improved CYP17 processivity is suggested to be the consequence of (otherwise rate-limiting) improved electron transfer efficiency towards CYP17. It explains the relatively high testosterone secretion during Leydig cell desensitization and is interpreted to be a protective mechanism to confine adverse consequences of enzyme decay.

17-alpha-Hydroxyprogesterone↗
PubMed1990

Postmenopausal androgen secreting ovarian tumour: pathophysiological implications; a case report.

Hyperandrogenism in women is usually accompanied by a disruption of the hypothalamic-pituitary-ovarian axis; however, the precise effect of chronically elevated androgens on this axis is poorly understood. We report a postmenopausal woman with a virilizing ovarian tumour in whom the effects of chronic testosterone secretion on the hypothalamic-pituitary axis was investigated. A 56-year-old woman was evaluated for hirsutism and hyperandrogenism of recent onset. Peripheral serum testosterone was high (19.4 nmol/l), while gonadotropins were below normal for a postmenopausal woman, FSH (19.7 IU/l) being higher than LH (10.3 IU/l). Four LH and 1 FSH pulse were detected over 4 h. A left intraovarian testosterone secreting tumour, shown by catheterization of the ovarian veins and containing imperfect crystalloids of Reinke, was excised. Postoperatively, peripheral testosterone became undetectable, while gonadotropins rose to normal postmenopausal values. This patient's LH/FSH ratio was less than 1, in contrast with other situations of chronic hyperandrogenism. This could be explained by the concomitant hypoestrogenic state, and/or the theoretical absence of inhibin. The interest of this case resides in that it constitutes an appropriate model for studying the effects of testosterone on LH and FSH secretion in the absence of the other two classically involved modulators, namely oestrogens and inhibin.

Androgens↗
PubMed1980

Androgen and estrogen production in elderly men with gynecomastia and testicular atrophy after mumps orchitis.

Gynecomastia developed in three men 1-30 yr after the occurrence of testicular atrophy due to mumps orchitis. At the time of study, these men were 63-68 yr of age. In these men the mean plasma production rate of testosterone was 816 microgram/24 h, a value 20% of that found in normal elderly men without gynecomastia. The plasma production rate of androstenedione averaged 1317 microgram/24 h. The mean production rates of 17 beta-estradiol and estrone in these subjects were 33 and 48 microgram/24 h, values comparable to those of normal young men. Extraglandular formation of estrogen from plasma prehormones accounted for all of the 17 beta-estridiol and most of the estrone produced by these elderly men with gynecomastia. Serum gonadotropin concentrations were elevated in these men, probably because plasma testosterone production rates were decreased. These findings are consistent with the view that the capacity of Leydig cells to secrete testosterone was impaired after mumps orchitis in these subjects, but the capacity to form estrogen was not similarly impaired, since most estrogen is formed in extraglandular sites. Thus, the impairment in Leydig cell testosterone secretion after mumps orchitis together with the normal increase in extraglandular aromatization that accompanies aging bring about a striking reduction in the ratio of testosterone to estrogen production rates, and gynecomastia may result.

Aged↗
PubMedDate not supplied

Developmental changes in in vitro testosterone production by dispersed Leydig cells during fetal life in rats.

The age-related evolution during fetal days 18.5-21.5 of the capacity of collagenase-dispersed Leydig cells to produce testosterone and to respond to LH or dibutyryl cyclic AMP (dcAMP) was studied in vitro in the rat. When dispersed Leydig cells were incubated in control medium, testosterone secretion by cells from 18.5-day-old fetuses during the first 5 h was 100 and 50% higher than secretion by cells from 20.5- and 21.5-day-old fetuses, respectively. The secretion maximally stimulated by 100 ng/mL LH or stimulated by 1 mM dcAMP was also stronger on day 18.5 than on days 20.5 and 21.5 during the first 3 h of culture. The dose-response curves for LH showed that the ED50 was similar for day 18.5 and 20.5 cells (2 ng/mL LH). During the course of 24-h incubation, the secretion rates also changed with time and fetal age: Between 5 and 24 h of culture basal secretion decreased in day 18.5 cells, rose slightly in day 20.5 cells, and increased sharply in day 21.5 cells; in the same way, in the presence of LH or dcAMP, the secretion by day 18.5 cells decreased faster than that of day 20.5 or 21.5 cells. The basal testosterone secretion of the Leydig cells and its maximum steroidogenic capacity decrease during late fetal life in the rat, and there was no change in the sensitivity to LH during this period. The age-related differences in the variations of the secretion rates as a function of the duration of incubation suggest the existence of an evolution in extragonadotropic regulations during late fetal life.

Animals↗
PubMed2003

Unilateral paramedian-sagittal brain cut extending from the level of the anterior commissure to the midlevel of the third ventricle above the amygdala affects gonadal function in male rat: a lateralized effect.

The aim of the present investigations was to study involvement of fiber systems to and from the insular cortex above the amygdala in the neural control of the hypophysio-testicular axis in male rats. Animals were subjected to a unilateral paramedian-sagittal brain cut above the amygdala, extending from the level of the anterior commissure to the midlevel of the third ventricle and causing among others partial deafferentation of the insular cortex. Right-sided cut induced a significant rise in basal testosterone secretion in vitro of both testes as compared to intact or sham-operated controls without affecting serum testosterone level. By contrast, left-sided cut slightly suppressed testicular steroidogenesis and significantly decreased serum testosterone concentration. In animals underwent sham or actual cut on either side, serum luteinizing hormone levels were similar, but significantly lower than those in intact controls. No change was observed in serum FSH concentration of any experimental group. The results indicate that afferent and efferent connections of the partially deafferented cortical regions including among others the insular cortex are involved in the control of testosterone secretion. The data further suggest functional laterality of the interrupted structures.

Amygdala↗
PubMed2002

Leptin in male reproduction: the testis paradigm.

Leptin, the adipocyte-derived hormone that plays a key role in body weight homeostasis, has recently emerged as a relevant neuroendocrine mediator in different systems, including the reproductive axis. Thus, compelling evidence points out a major role of leptin in the regulation of female pubertal development and fertility, both in humans and experimental animals. The contribution of leptin to the proper functioning of the male reproductive system has been less clear. However, data gathered in recent years, from independent groups and through a variety of experimental approaches, strongly suggest that leptin is able to act at different levels of the hypothalamic-pituitary-testicular axis. Herein, we review the biological effects and potential mechanisms of action of leptin upon rodent testis. Leptin appears to act as a direct inhibitory signal for testicular steroidogenesis, which may be relevant to explain the link between decreased testosterone secretion and hyperleptinaemia in obese men. Analysis of the molecular basis for leptin-induced inhibition of testosterone secretion revealed the potential involvement of decreased gene expression of several up-stream factors (e.g. SF-1, StAR and P450scc) in the steroidogenic pathway. In this context, testicular expression of leptin receptor (Ob-R) gene shows a complex pattern of alternative splicing with generation of multiple variants, including the functional leptin receptor type-b (Ob-Rb) and several short isoforms. Moreover, Ob-R mRNA expression in rat testis was regulated by homologous (leptin) as well as heterologous (gonadotropins) signals. Overall, the current data indicate that the testis is a direct target for leptin actions. Furthermore, the available evidence is suggestive of a tightly regulated, complex mode of action of leptin at different levels of the male gonadal axis that involves not only stimulatory but also inhibitory effects.

Animals↗
PubMed1980

[A comparative in vitro culture study of the action of the embryonic chick and rat testes on the embryonic chick Wolffian duct (author's transl)].

Embryonic chick and rat testes were cultured in vitro in combination with embryonic chick Wolffian ducts in order to compare their capacity for testosterone secretion. The rat testes stimulated the Wolffian ducts, whereas the chick testes did not. It is concluded that testosterone secretion of the embryonic chick testis is non-existent or negligible. This conclusion is in agreement with the findings of previous in vitro culture experiments. However, in the literature conflicting results were obtained by various authors when applying biochemical methods.

Animals↗
PubMed1989

Development of the inhibitory guanine nucleotide-binding regulatory protein in the rat testis.

The functional development of the inhibitory guanine nucleotide-binding regulatory protein (Gi) and anti-diuretic hormone (ADH) activity was investigated in rat testes. Adult (90-day-old), adolescent (40-day-old), prepubertal (23-day-old), and fetal (20.5 days of gestation) testis cells were cultured with 100 ng/ml pertussis toxin for 24 h. The cells were then cultured with human chorionic gonadotropin (hCG), the ADH agonist arginine vasotocin (AVT), or a combination of the two. Testis cells from rats 23, 40, and 90 days of age that were incubated with hCG increased testosterone production when compared with controls. Preincubation of the cells from postnatal rats with pertussis toxin significantly increased hCG-stimulated testosterone secretion when compared to cells preincubated in medium only at all three ages. AVT suppressed hCG-stimulated testosterone secretion, but this suppression was partially reversed in cells from all postnatal ages preincubated with pertussis toxin. Fetal testis cells showed no response to preincubation with pertussis toxin, even when levels were increased to 400 ng/ml or when pertussis toxin treatment was continued throughout the culture period. AVT also had no effect on fetal testis cells. These results indicate that the Gi protein and AVT are not functional in fetal testes but are active from prepubertal stages of development through maturity.

Animals↗
PubMed1993

Effects of GnRH analogues on pituitary-testicular function in free-ranging African elephants (Loxodonta africana).

We tested the ability of several GnRH analogues to suppress pituitary-testicular activity and potentially musth in free-ranging African elephants (Loxodonta africana). In Study 1, adult bulls were given 4 or 12 mg GnRH antagonist (Detirelix) or saline i.m. on day 0 (n = 3 bulls per treatment). Animals were then recaptured on day 2 (about 48 h later) and given 300 micrograms GnRH i.v. to assess the ability of the antagonist to block pituitary activity. Detirelix reduced (P < 0.05) basal concentrations of serum LH and testosterone on day 2 compared with day 0, with no effect of dose. Similarly, LH and testosterone release induced by GnRH were also reduced (P < 0.05) in the Detirelix-treated bulls (50-70% reduction in peak concentrations). In Study 2, elephants were given 30 mg of a structurally similar GnRH antagonist (103-201-40; n = 6), 22.5 mg of a long-acting GnRH agonist (Lupron Depot; n = 4) or D-mannitol carrier (n = 4) i.m. on day 0. All bulls were recaptured and given GnRH on day 2 (103-201-40 treatment) or on days 2 and 20 (Lupron Depot treatment) after the initial injection. In contrast to Detirelix, 103-201-40 did not inhibit basal or GnRH-induced LH or testosterone secretion. Pituitary-testicular responses to Lupron Depot were initially stimulatory, as evidenced by increased (P < 0.05) LH and testosterone secretion on days 0 and 2.(ABSTRACT TRUNCATED AT 250 WORDS)

Africa↗
PubMed1987

Biopotency and site of action of drugs affecting testicular steroidogenesis.

The effect of etomidate (an anaesthetic), epostane (WIN 32729; an inhibitor of ovarian and adrenal steroidogenesis) and cyproterone acetate (an antiandrogen) on testosterone secretion from mouse Leydig cells stimulated with LH (5 i.u./l) was tested. The concentration of drug which inhibited testosterone secretion by 50% was 11.5 +/- 1.1 (S.E.M.) mumol/l for cyproterone acetate, 1.2 +/- 0.2 mumol/l for etomidate and 0.23 +/- 0.03 mumol/l for epostane. The effect of all three drugs on testicular steroidogenesis was completely reversible. Thus testicular cells which had been washed after exposure to a greater than 95% inhibitory dose of drug responded in a similar manner to hormone stimulation as cells similarly washed and which had not been exposed to the drug. The sites of the antisteroidogenic effect of epostane, etomidate and cyproterone acetate were established using a method based on the sequential stimulation by the exogenous precursor steroids of the various steps leading to the biosynthesis of testosterone. It was concluded that etomidate acts at the sequence between LH binding and pregnenolone production, epostane acts at 3 beta-hydroxysteroid dehydrogenase and cyproterone acetate inhibits 3 beta-hydroxysteroid dehydrogenase and C17,20-lyase.

Androgen Antagonists↗
PubMed1978

Bromocriptine treatment of males with pituitary tumours, hyperprolactinaemia, and hypogonadism.

Plasma prolactin concentrations were measured in thirty-four males with pituitary tumours and twenty-two patients (65%) were found to have hyperprolactinaemia. Plasma testosterone concentrations were subnormal in twenty-nine patients. Ten patients with hyperprolactinaemia were treated with bromocriptine; prolactin was restored to normal values in eight patients but testosterone secretion remained deficient. Two patients were resistant to bromocriptine. Some improvement in libido and potency was obtained after restoration of normal prolactin concentrations in four cases in spite of persistently low testosterone secretion. For maximal improvement in sexual function treatment with both bromocriptine and testosterone was required.

Bromocriptine↗
PubMed1993

Liposome-mediated macrophage depletion: an experimental approach to study the role of testicular macrophages in the rat.

Liposome-entrapped dichloromethylene diphosphonate was injected locally into the right testes of adult rats. This treatment, which has been found to deplete resident macrophages in some other organs, reduced the number of testicular macrophages by at least 90%. Testicular weight and seminiferous tubule morphology were unaffected by liposome treatment. Leydig cell testosterone secretion gradually declined in the macrophage-depleted testes, and there was a compensatory increase in Leydig cell size and testosterone secretion in the contralateral saline-injected testes. These observations suggest that macrophages influence Leydig cell function locally. It is concluded that liposome-mediated depletion of testicular macrophages may serve as an experimental model with which to study the physiological role of these cells.

Animals↗