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At least 235 records · Page 13Linked to original sources
PubMed1997

Effects of chemotherapy-induced testicular damage on inhibin, gonadotropin, and testosterone secretion: a prospective longitudinal study.

To investigate the role of inhibin in the control of follicle-stimulating hormone (FSH) secretion, we have measured levels of immunoreactive inhibin (ir-inhibin), inhibin B, Pro-alpha C containing inhibins, FSH, luteinizing hormone (LH), and testosterone in twelve men with hematological malignancies before, during, and after chemotherapy. Inhibin B levels fell significantly by 1 month from a mean +/- SE baseline level of 273.2 +/- 32.8 pg/mL, reaching a nadir of 52.6 +/- 15.3 pg/mL at 4 months (P < 0.0001). FSH levels increased within the first month from a baseline level of 3.9 +/- 0.6 IU/L, reaching a peak level of 22.4 +/- 3.3 IU/L at 4 months (P < 0.0001). FSH and inhibin B were significantly and inversely correlated (r = 0.69, P < 0.0001). Pro-alpha C containing inhibin levels increased significantly (P < 0.05) at 3 months and were significantly and positively correlated with FSH (r = 0.38, P = 0.002). LH levels increased significantly but to a much lesser extent than FSH, the increase becoming evident only 4 months after treatment commenced (P < 0.03). Levels of ir-inhibin and testosterone remained unchanged throughout the study. These data provide strong support to the hypothesis that inhibin B is the physiologically important form of inhibin in men, negatively regulating FSH secretion at the pituitary. Furthermore, they suggest that FSH stimulates inhibin alpha-subunit secretion by the testis.

Adult↗
PubMed2001

Selective testosterone secreting adrenocortical carcinoma in an infant.

Adrenocortical carcinoma in children is a rare tumor of adrenal gland. An infant presented with signs of virilization due to selective testosterone hypersecretion. Diagnosis was established with the help of the computerized tomographic scan and histopathological examination. Following adrenalectomy patient made uneventful recovery and six months later does not have any clinical or laboratory evidence of recurrence or metastasis.

Adrenal Cortex Neoplasms↗
PubMed1988

Effect of a traditional herbal medicine (shakuyaku-kanzo-to) on testosterone secretion in patients with polycystic ovary syndrome detected by ultrasound.

In 20 infertile Japanese with polycystic ovary syndrome Shakuyaku-Kanzo-To was used to lower plasma testosterone levels and hence to induce pregnancy. The polycystic ovary was classified into two types; general cystic and peripheral cystic patterns. Plasma testosterone was decreased in 18/20 (90%) and 5/20 (25%) became pregnant. The plasma testosterone concentration in the case of the general cystic pattern was significantly higher than that of peripheral cystic pattern, and the pregnancy rate in those with the general cystic pattern was lower. The efficacy of Shakuyaku-Kanzo-To therefore seems to vary according to the type of polycystic ovary syndrome treated.

Drug Evaluation↗
PubMed1986

Missing effect of etomidate on testosterone secretion in man.

We studied the effect of low dosage (0.26 mg/kg as a single induction dose) and high dosage (30 mg/h for long term sedation) etomidate on serum testosterone and serum luteinizing hormone (LH) concentrations in males. During high dose etomidate we found inhibition of both 11 beta-hydroxylase and cholesterol-side-chain cleavage enzyme with unresponsiveness of progesterone, 17 alpha OH-progesterone and 11-deoxycortisol to stimulation with ACTH. However, neither high dosage nor low dosage etomidate had any influence on serum testosterone or LH concentrations. We conclude that, in contrast to other substituted imidazole derivatives, etomidate does not interfere with testicular testosterone synthesis. It therefore may be possible to find clinically useful imidazole derivatives with endocrine actions confined to either the adrenals or the testes.

17-alpha-Hydroxyprogesterone↗
PubMed1977

Cannabinoids inhibit testosterone secretion by mouse testes in vitro.

Addition of delta-9-tetrahydrocannabinol or cannabinol to an incubation medium containing decapsulated mouse testes caused a significant reduction in the accumulation of testosterone in the medium. This result suggests that the reported effects of cannabis on male sexual and reproductive function may result from direct inhibition of testicular steroidogenesis by both psychoactive and nonpsychoactive constituents of marihuana.

Aging↗
PubMed1984

[The problem of testosterone secretion by the chick embryo testis: new research].

The aim of this study was to determine whether the chick embryo testis was able to convert dehydroepiandrosterone and androstenedione into testosterone. Testes from 17-19 day old chick embryos were cultured in vitro in the presence of tritiated dehydroepiandrosterone or androstenedione of high specific activity, and the radioactive testosterone formed was isolated by thin-layer chromatography and identified by recrystallization to constant specific activity. Parallel experiments with mouse embryo testes showed that these methods were valid. However, since specific activity with chick embryo testes was very low and could not be brought to constancy, testosterone could not be identified with these testes. It is concluded that the 17-19 day old chick embryo testis cannot form testosterone from either dehydroepiandrosterone or androstenedione. This conclusion is in keeping with the absence of a physiological role for testosterone in the male chick embryo.

Androstenedione↗
PubMed2004

Pulsatile intravenous infusion of recombinant human luteinizing hormone under acute gonadotropin-releasing hormone receptor blockade reconstitutes testosterone secretion in young men.

The present study tests the hypothesis that iv infusion of discrete pulses of recombinant human (rh)LH after overnight GnRH-receptor blockade can restore midphysiological concentrations of testosterone (Te) in normal young men. In a pilot time-course analysis, injection of the GnRH antagonist ganirelix (2.0 mg sc) at 2200 h lowered LH concentrations (mean +/- sem) from 3.4 +/- 0.7 to 0.8 +/- 0.1 IU/liter (P < 0.01) and Te concentrations from 416 +/- 48 to 107 +/- 16 ng/dl (P < 0.01) (to convert to nmol/liter, multiply by 0.0347) at 0800 h the next morning. LH and Te concentrations remained suppressed thereafter for an additional 15 h (interval, 10-25 h after ganirelix administration) at mean values of 1.2 +/- 0.1 IU/liter and 67 +/- 10 ng/dl, respectively (P < 0.005 vs. baseline). Based on these data and earlier dose-finding studies, eight men received a single ganirelix injection followed by seven consecutive iv pulses of rhLH (15.3 IU Second International Reference Preparation) each delivered over 6 min every 2 h beginning at 0800 h. Recurrent rhLH stimuli restored mean LH concentrations (IU/liter of homologous standard) to 4.8 +/- 0.3, LH peak maxima to 7.1 +/- 0.6, incremental LH peak amplitudes to 3.7 +/- 0.4, and interpeak nadir LH concentrations to 3.3 +/- 0.3 (each P < 0.01 vs. saline infusion after ganirelix). These values were indistinguishable from the normal 95% range established in 23 young adults of comparable age. Injected LH pulses increased total Te concentrations (ng/dl) to 440 +/- 52, Te peak maxima to 552 +/- 64, incremental Te amplitudes to 188 +/- 23, and interpeak nadir Te concentrations to 366 +/- 43 (each P < 0.01 vs. saline addback; P value not significant vs. untreated men). Under combined ganirelix inhibition and pulsatile rhLH drive, Te concentrations rose from a nadir of less than 120 ng/dl to an asymptotic plateau of 611 ng/dl with an estimated half-time of 97 +/- 9.1 min. Cross-correlation analysis of paired serial LH and Te concentrations verified that infused LH pulses stimulate Te elevations within 40-70 (median 50) min (P < 0.001). Kinetic estimates of the half-life of exogenous rhLH averaged 107 +/- 3.8 min, which value exceeded that of secreted LH monitored after pharmacological GnRH stimulation (83 +/- 12 min; P = 0.012). We conclude that intermittent iv pulses of rhLH delivered over 12 h under selective GnRH-receptor blockade can restore young adult-like pulsatile LH and Te concentrations with an appropriate time delay coupling the lutropic stimulus to the steroidogenic response. Whether a comparable near-physiological paradigm can maintain human Leydig-cell testosterone production for a more extended interval is not known.

Adolescent↗
PubMed1984

Role of catecholamines in the inhibitory effect of immobilization stress on testosterone secretion in rats.

Immobilization stress applied for 6 h induced, in adult male rats, a rise of epinephrine (E) and norepinephrine (NE) plasma levels and a decrease of baseline plasma testosterone (T) values and of human chorionic gonadotropin (hCG)-induced T response. Treatment of the animals for 5 weeks with guanethidine (G), a sympathetic neuron toxic agent, significantly decreased E and NE responses to stress and partly antagonized the inhibitory effects exerted by immobilization on T biosynthesis. Adrenalectomy totally suppressed circulating E and reduced the stress-induced NE increase while partly antagonizing the inhibitory effects exerted on T biosynthesis. Combined G and adrenalectomy treatments totally suppressed plasma E and NE, and completely blocked the effects of immobilization on T levels. Treatment of the animals with the alpha 1-adrenergic blocker, prazosin, and the beta 1-adrenergic blocker, metoprolol, did not modify the effects of stress on T biosynthesis. Treatment with propranolol or with butoxamine, a nonspecific beta- and a specific beta 2-adrenergic receptor blocker, respectively, antagonized the testicular hyposensitivity to hCG induced by stress. Stress- or treatment-induced changes of plasma luteinizing hormone (LH) and hCG levels were not consistently correlated with plasma T modifications. These findings suggest that at least part of the inhibitory effects of immobilization stress on T biosynthesis is exerted by catecholamines through a beta 2-adrenergic receptor.

Adrenal Glands↗
PubMed1983

Effects of sulpiride induced hyperprolactinemia on testosterone secretion and metabolism before and after HCG in normal men.

The purpose of the study was to investigate the effects of sulpiride-induced hyperprolactinemia on testicular functions, as assessed by evaluation of plasma testosterone (T), dihydrotestosterone (DHT) and 17 beta-estradiol (E2) levels. An HCG test (5000 IU on three consecutive days) was performed in basal conditions and after 12 and 26 days of sulpiride treatment (150 mg daily) in 7 male volunteers, 19 to 32 years of age, as well as in 6 sulpiride-free controls. The results show that after 12 days of induced hyperprolactinemia (mean increase 400%) the T response to HCG was similar to basal test; after 26 days however, the increase of T mean plasma levels was significantly greater. The increase in E2 significantly correlated to that of T during the first and second HCG tests, but no longer after 26 days of hyperprolactinemia, resulting in an imbalance of the E2/T ratio of plasma increments. The response of DHT to HCG was significant in basal conditions and after 26 days of sulpiride and always correlated with T behavior. Data obtained in our experimental conditions suggest that PRL might enhance T secretion. 5 alpha-reductase activity seemed to be partially affected after 12 days of treatment, while a significant inhibition seemed to be exerted on aromatase activity.

Adult↗
PubMed1991

Stimulatory effects of alpha-hANP on testosterone secretion in man.

Several recent observations suggest that atrial natriuretic peptides (ANP) can modulate steroidogenesis in isolated rat Leydig cells. At present, it is unknown whether ANP influence human testicular steroidogenesis. We therefore evaluated the effects of alpha-human ANP (hANP) administration on testosterone plasma levels in peripheral and internal spermatic venous blood of young men (catheterized for contrast study of varicocele). Six subjects were injected with 100 micrograms alpha-hANP in the cubital vein. Six different patients similarly received 50 micrograms LHRH. Three controls received 2 ml saline. Plasma LH, FSH, and testosterone were then determined 15 min before, at time of injection, and 15, 30, 45, and 60 min thereafter in spermatic vein and peripheral venous blood, as well as at 120 min in peripheral blood. LHRH--induced LH increase was followed by a marked increase of spermatic vein testosterone concentrations, but the peripheral testosterone concentration did not increase. Similarly, alpha-hANP administration did not affect peripheral testosterone and LH concentrations, but significantly increased spermatic vein testosterone levels (P less than 0.01). Our findings demonstrate that alpha-hANP exerts its stimulatory effect on testicular steroidogenesis in man without modifying gonadotropin secretion, suggesting that alpha-hANP may directly influence Leydig cell function.

Adolescent↗
PubMed1984

Reduced pulsatile luteinizing hormone and testosterone secretion with aging in the male rat.

To identify possible age-dependent changes in the feedback relationship between the brain-pituitary and testes, we examined the minute-to-minute patterns of plasma luteinizing hormone (LH) and testosterone (T) in intact, young male rats and compared these profiles to those of old animals. Young (3 mo; n = 11) and old (22 mo; n = 12) Sprague-Dawley rats were fitted with indwelling venous catheters and between 24 and 48 h later, were bled without anesthesia, by remote sampling, at 10-min intervals for 8 h. Blood samples of 400 microliter were withdrawn, and an equivalent volume of a blood replacement mixture was infused after each sample. Plasma LH and T levels in each sample were measured by radioimmunoassay (RIA). Plasma T levels in old animals failed to show the transient oscillations observed in young animals. Mean plasma T levels were 50% lower in old compared to young animals (P less than 0.001). Plasma patterns of LH in old animals, like their younger counterparts, showed statistically significant episodic increases, whose apparent pulse frequency was inappropriately low for their circulating T level (although not statistically different from the young group). Pulse amplitude in the old animals was 66% lower in the old compared to the young group (P less than 0.015). We conclude that age-associated alterations in brain mechanisms governing LH secretion underline these endocrine changes.

Aging↗
PubMed1997

Increased testosterone secretion in bulls treated with a luteinizing hormone releasing hormone (LHRH) agonist requires endogenous LH but not LHRH.

The requirement for endogenous LHRH and LH action in the maintenance of elevated plasma concentrations of testosterone in bulls receiving the LHRH agonist deslorelin was examined. In Experiment 1, bulls were either (i) left untreated (control); (ii) implanted with deslorelin; (iii) actively immunized against LHRH; or (iv) implanted with deslorelin and immunized against LHRH. Experiment 2 was of similar design to Experiment 1, except that bulls were immunized against LH in place of LHRH. In Experiment 1, plasma LH declined in bulls immunized against LHRH, but not in the bulls immunized against LHRH and implanted with deslorelin. Also in Experiment 1, plasma testosterone declined in bulls immunized against LHRH but was elevated in bulls treated with deslorelin and bulls treated with deslorelin and immunized against LHRH. In Experiment 2, bulls immunized against LH and treated with deslorelin had plasma concentrations of testosterone similar to controls, whereas bulls treated only with deslorelin had elevated plasma testosterone. It was concluded from these experiments that endogenous LHRH action was not required for increased steroidogenic activity in bulls treated with a LHRH agonist. However, circulating LH was necessary for increased plasma testosterone in bulls implanted with deslorelin. LH is therefore involved in mediating the response of bulls to treatment with deslorelin, either by acting directly at the testes or through a permissive role that allows a direct action of deslorelin at the testes.

Animals↗
PubMed1999

Diurnal rhythms of luteinizing hormone, follicle-stimulating hormone, and testosterone secretion before the onset of male puberty.

To investigate hormonal change before the onset of male puberty, we measured LH and FSH in serum samples drawn every 20 min for 24 h and measured testosterone hourly for 24 h. Forty-six boys (32 prepubertal and 14 pubertal) of short stature, between 4.4-19.3 yr of age, participated in this study. LH and FSH were measured using a time-resolved immunofluorometric assay, and testosterone was measured using high sensitivity RIA capable of detecting a testosterone concentration of 0.01 ng/mL. Diurnal rhythms of LH, FSH, and testosterone were apparent in all subjects, including those aged 4-5 yr. Serum LH and FSH concentrations showed night-day variation in a pulsatile fashion. The serum testosterone concentration was elevated at early morning in all subjects. Mean 24-h LH, FSH, and testosterone concentrations of prepubertal subjects who did not attain puberty for at least 3 yr were 0.10 U/L, 0.63 U/L, and 0.06 ng/mL, respectively, whereas those of prepubertal subjects who attained puberty within 1 yr (0.54 U/L, 1.68 U/L, and 0.10 ng/mL, respectively) were significantly higher. Furthermore, mean 24-h LH, FSH, and testosterone concentrations increased with developing puberty. All of the 46 subjects showed positive cross-correlation between the LH and testosterone time series. The mean lag time from the LH to the testosterone time series in the prepubertal subjects who attained puberty within 1 yr (4.7 +/- 2.4 h, mean +/- SD) was shorter than that in the prepubertal subjects who attained puberty after at least 3 yr (7.3 +/- 2.2 h). This lag time decreased with developing puberty, plateauing at 1.4 +/- 0.9 h at midpuberty. Thus, the diurnal rhythms of LH, FSH, and testosterone already exist at 4-5 yr of age; serum LH, FSH, and testosterone levels increase before the onset of puberty; and a time delay is observed between the LH and testosterone time series that decreases before the onset of puberty.

Adolescent↗