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 1,585 records · Page 88Linked to original sources

Inhibition of aldosterone production by testosterone in male rats.

In vivo and in vitro experiments were designed to assess the effect of testosterone on aldosterone secretion in male rats. Orchidectomized rats were injected subcutaneously with oil or testosterone propionate ([TP] 2 mg/kg) for 7 days. Intact rats were injected with oil only. The results indicate that the plasma aldosterone level was higher in orchidectomized versus intact and TP-replaced rats. In the in vitro study, testosterone caused a marked decrease of aldosterone secretion by zona glomerulosa (ZG) cells, but failed to alter the accumulation of intracellular adenosine 3',5'-cyclic monophosphate (cAMP). Testosterone significantly decreased the corticotropin (ACTH)-stimulated production of aldosterone and accumulation of cAMP in rat ZG cells. The conversion of corticosterone to aldosterone and of 25-OH-cholesterol to pregnenolone, as well as angiotensin II (ANG II)-stimulated production of aldosterone, were decreased by testosterone. These results suggest that testosterone inhibits the basal and ANG II- and ACTH-stimulated release of aldosterone, via inhibition of aldosterone synthase activity and cytochrome P-450 side-chain cleavage (P450scc) activity, and ACTH-stimulated cAMP accumulation in rat ZG cells.

1-Methyl-3-isobutylxanthine↗

Effects of 4-tert-octylphenol, 4-tert-butylphenol, and diethylstilbestrol on prenatal testosterone surge in the rat.

In the present study, we evaluated the effects that 4-tert-octylphenol (OP) and 4-tert-butylphenol (BP) had on the prenatal testicular testosterone surge at embryonic day (ED) 19.5 in the rat. In utero exposure to alkylphenols (0.1-100 mg/kg maternal weight) on EDs 13.5, 15.5, and 17.5 did not decrease testicular testosterone content, whereas exposure to diethylstilbestrol (DES) caused a significant depression in testosterone synthesis and secretion. The depression was maintained during ex vivo tissue culture. In order to elucidate the observed differences in the in vivo effects between alkylphenols and DES, the exposures were also carried out in tissue culture of intact ED 19.5 testes. Basal testosterone, progesterone, cAMP production and hCG-induced testosterone levels were determined during and after a 3-h culture period. DES (100 mg/l) did not alter testosterone production but caused a two-fold increase in progesterone. OP (10, 100, 500 mg/l) and BP (100 mg/l) significantly increased testosterone and progesterone levels by up to seven-fold. In the presence of BP 100 mg/l, however, the intratesticular testosterone content did not correlate with the significantly increased fraction of secreted, or leaked, testosterone. The latter was correlated with tissue damage observed at electron microscopic level. Consistent with this, BP 500 mg/l elevated testicular testosterone level slightly during the first hour in the culture but the level subsequently returned to the control value. At the electron microscopic level, alkylphenols caused most severe changes in Leydig cell membrane structures and lipid droplets. In the DES-treated testes, membrane vesicle formation around the lipid droplets and increased mitochondrial pleiomorphy were observed. Altogether, the present in vivo and in vitro analyses confirm different effects of alkylphenols and DES on fetal rat steroidogenesis and tissue structure.

Animals↗

Cortisol and androgen secretion in a case of Nelson's syndrome with paratesticular tumors: response to cyproheptadine therapy.

Bilateral paratesticular tumors were observed in a 32-yr-old man 14 yr after he developed a pituitary tumor after adrenalectomy for Cushing's disease (Nelson's syndrome). Plasma ACTH concentrations were markedly elevated (mean, 6350 pg/ml), but urinary free cortisol concentrations were low (27-31 micrograms/24 h). Catheterization revealed a spermatic to peripheral venous gradient for cortisol consistent with secretion of this steroid by the tumor. This was confirmed by decreased cortisol excretion after tumor excision. Serum androgen (testosterone, androstenedione, dihydrotestosterone, and dehydroepiandrosterone-sulfate) and progestin (progesterone and 17-hydroxyprogesterone) concentrations were decreased and did not decline further after tumor removal. These latter observations suggested that the paratesticular tumors did not secrete appreciable testosterone or any of its immediate precursors. Serum gonadotropin levels were also low. Cyproheptadine treatment resulted in a marked lowering of plasma ACTH concentrations (221-320 pg/ml). This was associated with an increase in both plasma LH and testosterone concentrations. These observations are consistent with the hypothesis that ACTH may directly affect LH and testosterone secretion.

Adrenalectomy↗

Androgen-dependent beard dermal papilla cells secrete autocrine growth factor(s) in response to testosterone unlike scalp cells.

Androgens stimulate many hair follicles, e.g., beard, but may cause regression on the scalp; occipital areas are considered androgen independent. The mesenchyme-derived dermal papilla that regulates the hair follicle is considered the site of androgen action. Because hair size has been clearly related to dermal papilla size, one of the key functions androgens must regulate is the size of the dermal papilla. This implies that androgens stimulate dermal papilla cells to divide or to secrete autocrine mitogenic factors. As physiologic levels of androgens do not stimulate mitogenesis in cultured dermal papilla cells, this study was designed to determine whether dermal papilla cells cultured from human hair follicles with different responses to androgens in vivo, i.e., androgen-dependent beard and androgen-independent nonbalding scalp, produce soluble autocrine mitogenic factors and, if so, whether either cell type altered their secretion in response to testosterone in vitro. Conditioned medium was prepared by incubating individual primary lines of cells for 24 h with, and without, testosterone (10(-10)-10(-5) M). All conditioned media significantly increased [3H] thymidine incorporation by other dermal papilla cells; trypsin treatment significantly reduced the effect. Although both beard and scalp cell conditioned media had a similar stimulatory potential, beard cells incorporated approximately double the [3H]thymidine of scalp cells, in both types of media. Physiologic levels of testosterone increased mitogenic factor production by beard, but not scalp cells; only beard cells responded to these factor(s). Testosterone added after conditioning had no effect, indicating stimulation was not a synergistic effect of testosterone and conditioned medium. Thus, both beard and scalp cells release similar autocrine growth factor(s), but their response to these factor(s) is determined by their in vivo origin. Testosterone in vitro stimulates secretion of an autocrine growth factor(s) by beard, but not scalp cells, to which only beard cells are able to respond, reflecting the responses to androgens in vivo. These factors may be involved in the key increase of dermal papilla size necessary for androgen-induced changes in hair size.

Adult↗

[Do androgens modulate luteinizing hormone secretion in women?].

In hyperandrogenic states an abnormal pattern of LH secretion in women is observed, which is presumed to result from a direct action of androgen or its conversion to estrogen. Two strategies are available to study the effect of testosterone on LH secretion. One involves the use of non-steroidal compounds that block the negative feedback actions of endogenous androgens by binding to androgen receptors; the other consists only in the administration of androgens. Following these two strategies, we first studied the pulsatile gonadotrophin secretion in hyperandrogenic women, following flutamide administration, a specific androgen receptor blocker. Flutamide treatment was followed by a decrease in LH pulse amplitude and mean LH concentrations, demonstrating that androgen receptor blockade reduces LH secretion in hyperandrogenic women. To establish the level at which the androgen effect is exerted, we further studied the acute effect of testosterone (hyperandrogenic levels) and the blockade of its receptor on LH secretion in patients with severe hypothalamic deficiency treated with pulsatile GnRH (GnRHp). LH pulse profiles were assessed under GnRHp treatment alone, during testosterone and during testosterone and flutamide administration. Testosterone increased LH secretion and LH pulse amplitude. Flutamide significantly reverted the LH increase induced by testosterone. These results strongly suggest that testosterone in the hyperandrogenic female range, may facilitate LH secretion by the pituitary, effect that is reversed by the blockade of the androgen receptor.

Androgens↗

The use of testosterone as a male contraceptive.

Testosterone functions as a contraceptive by suppressing secretion of the pituitary gonadotropins luteinizing hormone and follicle stimulating hormone. Low levels of these hormones decrease endogenous testosterone secretion from the testis and deprive developing sperm of the signals required for normal maturation. Interference with sperm maturation causes a decline in sperm production and can lead to reversible infertility in men, raising the possibility that testosterone could be utilized in a commercially available contraceptive. To this end, testosterone has been studied alone and in combination with either gonadotropin releasing hormone analogues or progestins in efforts to improve its contraceptive efficacy. In this chapter, we will review efforts to use testosterone to create a safe, convenient, efficacious contraceptive method for men.

Contraception↗

Steroid secretion by follicles and cysts from the hypothyroid, hCG-treated rat.

Hypothyroid rats develop cystic follicles after daily administration of human chorionic gonadotropin (hCG). This study was undertaken to compare progesterone, testosterone, and estradiol secretion by antral follicles (0.9-1.0 mm) and cysts (small; 1.2-2.0 mm; large: > 2.0 mm) from hypothyroid, hCG-treated rats with that of antral follicles from euthyroid, saline-treated animals. After 3, 5, or 10 days of hCG injections, follicles and cysts were dissected from the ovaries, diameter determined, and incubated in minimum essential medium (MEM) for 2 hr at 37 degrees C. Media were assayed for progesterone, testosterone, and estradiol by RIA. Progesterone secretion by antral follicles removed after 3, 5, or 10 days was similar but small cysts secreted significantly more of this steroid than did antral follicles. Large cysts secreted significantly more progesterone than all other follicles and cysts. After 10 days of treatment with hCG, antral follicles from hypothyroid, hCG-treated rats secreted two to three times more testosterone than similar follicles from euthyroid, saline-treated animals. Changes in estradiol secretion were not apparent until after 10 days of hCG treatment. Both small and large cysts from those animals secreted significantly more estradiol than all other follicle and cyst groups. These results suggest that steroid secretion by follicles and cysts could be contributing to elevated serum levels of progesterone and testosterone during the first 10 days of cyst induction. However, cysts may be contributing estradiol only during the later stages of cyst induction.

Animals↗

Abolition of the seasonal release of luteinizing hormone and testosterone in Alpine male goats (Capra hircus) by short photoperiodic cycles.

This study was performed to determine whether rapid alternation between long and short days abolished seasonal variations in the activity of the hypothalamo-pituitary-testis axis observed normally in Alpine and Saanen male goats during the year. Three groups of 6 males were used: group 1 remained in open sheds under the natural annual change in daylength from 16 h of light (long day) to 8 h of light (short day). Group 2 was exposed to 1 month of long days alternated with 1 month of short days; and group 3 to 2 months of long days alternated with 2 months of short days. In group 1, blood samples were taken in December, February and June; in groups 2 and 3, samples were obtained once during short and long days for the melatonin assay. For luteinizing hormone and testosterone determinations monthly samples from group 1 were obtained from September to August while, in groups 2 and 3, blood samples were taken on 4 occasions during long and short days. Weekly blood samples were taken from all groups during the whole of the experiment to measure prolactin and testosterone concentrations. Melatonin profiles indicated that secretion by the pineal gland of male goats from the treated groups adapted to rapid changes in daylength: duration of nocturnal secretion was close to that of the dark period. Treated goats were also able to transduce this signal adequately and always responded to long days by increasing their prolactin concentration (mean +/- s.e.m.; group 2: 62.4 +/- 6.8 ng/ml; group 3: 102.3 +/- 15.7 ng/ml) and to short days with a decrease in prolactin concentrations (35.0 +/- 3.6 and 46.1 +/- 9.5 ng/ml, respectively). In the treated groups, luteinizing hormone pulse frequency varied with day length. In group 2, it was higher in long days (1.1 +/- 0.3 pulses in 8 hours) than in short days (0.7 +/- 0.3) while, in group 3, this frequency was higher in short days (1.9 +/- 0.3) than in long days (0.5 +/- 0.2). Testosterone secretion also varied with daylength; in group 2, the testosterone concentrations were maximum during long days (5.8 +/- 1.4 ng/ml) while in group 3 the maximum testosterone concentrations occurred during short days (6.4 +/- 1.2 ng/ml). These results lead to the conclusion that rapid alternation of long and short days either attenuated (group 3) or prevented (group 2) seasonal changes in the activity of the hypothalamo-pituitary axis.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

Compensatory response of the luteinizing-hormone (LH)-releasing hormone (LHRH)/LH pulse generator after administration of a potent LHRH antagonist in the ram.

It is established that the blockade of the pituitary LHRH receptor by an LHRH antagonist will suppress pituitary LH secretion and reduce serum concentrations of gonadal steroids. Little is known, however, about the activity of the LHRH/LH pulse generator during this inhibitory period or during the recovery phase. To investigate this, a potent LHRH antagonist [N-Ac-D-pCl-Phe1,D-pCl-Phe2,D-Trp3,D-hArg(Et2)6, D-Ala10 LHRH was injected iv into sexually active rams and the changes in the blood plasma concentrations of LH, FSH, testosterone, and PRL were measured in samples collected every 15 min for 24-48 h. The treatment induced an immediate blockade of pulsatile LH secretion and a parallel decline in blood levels of testosterone. Plasma levels of FSH were not suppressed by treatment with the LHRH antagonist and there was no consistent effect on plasma levels of PRL. The duration of the inhibition of LH was dose dependent lasting 4.3 +/- 0.4 h, 18.0 +/- 1.0 h, and 31.8 +/- 1.3 h for the low (6 micrograms/kg), medium (36 micrograms/kg), and high (365 micrograms/kg) doses of LHRH antagonist, respectively. During the recovery period there was an approximate 2-fold increase in the frequency of LH pulses. These results suggest a compensatory response to the decline in the negative feedback effect of testosterone secretion. Even the lowest dose of antagonist elicited a decrease in the level of testosterone and an increase in LH pulse frequency. At this dose, the decline in testosterone was very transitory indicating an acute sensitivity of the hypothalamus to changes in the negative feedback signal. These results suggest that the suppression of LH and testosterone secretion in the ram by LHRH antagonist is associated with a compensatory increase in the activity of the LHRH pulse generator.

Animals↗

Exogenous oestrogen affects calcium metabolism differently from exogenous testosterone in ovariectomized or orchiectomized rats fed a high fructose diet severely deficient in magnesium.

To investigate interactions between sex hormones, dietary fructose, and a severe magnesium deficiency on calcium metabolism, 10 week old ovariectomized (OVX) female, and orchiectomized (ORX) males rats were studied. The OVX and ORX animals were divided into two groups: one half of the animals in each group was injected with beta-oestradiol-3-benzoate dissolved in sesame oil twice a week; the other half was injected with testosterone cypionate in sesame oil twice a week. All animals were pari-fed a severely magnesium-deficient fructose diet. After a 4 week experimental period, a 24 h urine sample was collected for measurements of cAMP, calcium, magnesium, and phosphorus. Blood was collected for determination of calcium, magnesium, phosphorus, 25-hydroxy- and 1.25-dihydroxycholecalciferol [25(OH)D, 1.25(OH)2D], and parathyroid hormone (PTH). Femurs were used for measurements of bone mineral content (BMC) and density (BMD). Oestrogen treatment produced hypercalcaemia and hypercalciuria, and, further, this was higher in female than in male rats. In contrast, testosterone treatment produced hypocalcaemia and hypocalciuria. Hypocalcaemia in testosterone-treated animals may stimulate secretion of PTH. Testosterone-treated animals had significantly lower BMD than oestrogen-treated animals. High circulating PTH seemed to cause bone loss in the testosterone group. High PTH may stimulate hydroxylation of 25(OH) D to 1.25(OH)2D in the kidneys, and high circulating 1.25(OH)2D would antagonize bone formation. Either endogenous or exogenous oestrogen increased kidney calcification. The study indicates that oestrogen-fructose-magnesium interaction on calcium metabolism was significantly different from that of testosterone.

Anabolic Agents↗

Effects of orchidectomy and testosterone replacement treatment on pulsatile luteinizing hormone secretion in the adult rhesus monkey (Macaca mulatta).

The effect of bilateral orchidectomy and subsequent replacement treatment with testosterone (T) on the intermittent pattern of LH release were studied in six adult male rhesus monkeys. Frequent blood samples were withdrawn for extended periods via remote sampling devices that permitted continuous access to the venous circulation with minimal restraint of the animals. Plasma concentrations of LH were determined by RIA, and episodes of LH secretion (pulses) were identified using a computer-executed algorithm. In intact animals, the frequency of episodic LH secretion averaged one pulse every 4.5 h, and this increased within 2 days of castration to approximately one pulse every hour. The acceleration in LH pulse frequency occasioned by orchidectomy was associated with increases in mean plasma LH concentration and an enhancement of LH pulse amplitude. Implantation of acutely orchidectomized animals with T-containing Silastic capsules that resulted in sustained increments in plasma T concentrations in the mid to upper physiological ranges generally resulted, within 10 days, in a partial to complete reversal of the high LH pulse frequency characteristic of the castrated animal. The onset of the T-induced reduction in LH pulse frequency was associated with a marked increase in pulse amplitude. Since it is generally held that a LH pulse is occasioned by, and therefore reflects, a discharge of hypothalamic gonadotropin-releasing hormone, it may be proposed that in the rhesus monkey, the testes impose a decisive retardation on the neural mechanism that governs the timing of intermittent gonadotropin-releasing hormone secretion, and that this modulation of the hypophysiotropic oscillator by the gonad is mediated by testicular T secretion.

Animals↗

Large and small cells of the porcine corpus luteum: differential capacity to secrete estradiol and aromatize exogenous androgen during mid- and late luteal phase.

It has been demonstrated previously that aromatization capacity of luteal cells increased as the luteal phase progresses, suggesting that estradiol secretion by regressing corpora lutea could play an active role in regulation of the estrus cycle. To determine whether a specific luteal subpopulation is responsible for this process, luteal cells collected from mature (8-10 days after ovulation) corpora lutea were separated at unit gravity into small (14-26 microns) and large (26-38 microns) cell types. Aliquots of separated cells were incubated overnight in M199 medium alone (= control) or in medium containing: 10 M-5 T, 10(-6) M or 10(-7) M T or 0.1 x 10(-3) M, 0.5 x 10(-3) M or 1 x 10(-3) M aromatase inhibitor CGS 16949A. Both cell types were capable of estradiol production without the addition of substrates. The endogenous content of estradiol was always higher in large granulosa-derived luteal cells (LC) than in small theca-derived luteal cells (SC), and was higher in the late (LLP) than in the mid-luteal (MLP) phase. Both types of cells responded to testosterone by increasing estradiol secretion. Adding aromatase inhibitor to LC isolated from MLP and LLP decreased testosterone-stimulated estradiol secretion. On the other hand, aromatase inhibitor had no effect on testosterone-stimulated estradiol secretion by SC isolated during MLP, and inhibited testosterone-stimulated estradiol secretion by SC isolated during LLP. These data are the first to show the ability of both populations of porcine luteal cells to aromatize exogenous testosterone. The observed lack of aromatase inhibitor influence upon basal secretion of estradiol by SC separated from mature corpora lutea, and the decrease of testosterone-stimulated estradiol secretion by SC isolated from regressing corpora lutea, indicate that cytodifferentiation during luteinization could cause expression of P450arom in theca-derived luteal cells.

Androgens↗

[Effect of adrenocorticotropic hormone on the secretory activity of the gonads and adrenals of male hamadryas baboons].

The time course of the secretion of steroid hormones to the adrenal and seminal veins following administration of synthetic ACTH was studied in experiments on mature male hamadryas baboons. Testosterone, 5 alpha-dihydrotestosterone, androstendion, 17-oxyprogesterone and 17-oxypregnenolone levels in the venous blood were determined by means of radioimmunoassays with preliminary chromatographic isolation of steroids on cellite. The rate of hormone secretion by the adrenal and seminal glands was calculated by the gradient of the hormone concentration in the peripheral blood and in the blood outflowing from the steroid secreting glands. Sharp activation of the seminal secretion of testosterone, 5 alpha-dihydrotestosterone, androstendion and 17-oxyprogesterone was recorded 10-30 min after ACTH administration. The time course of testosterone secretion by the testes in ACTH administration showed correlation with changes in the hormone concentration in the peripheral blood. The data obtained were indicative of the seminal origin of a short-term rise of testosterone concentration in male hamadryas baboons in the initial period of ACTH action. A possible mechanism of the ACTH effect on the biosynthesis of steroids in the testes was discussed.

Adrenal Glands↗

The capability of androgen aromatization by bank vole Leydig cells in vitro: the effect of aromatase inhibitor.

The effect of increasing concentrations of aromatase inhibitor CGS 16949A on LH- and testosterone-supplemented estradiol secretion by Leydig cells was studied. Leydig cells were obtained from immature and mature bank voles, which were reared in a long or a short photoperiod conditions. They were either incubated for 6 hrs with LH and/or testosterone (LH/testosterone-supplemented cultures), or as the control cultures. Aromatase inhibitor was added for further 18 h. After 24-h incubation period testosterone and estradiol secretion were radioimmunologically examined. This study revealed that in bank voles, Leydig cells' aromatase activity appeared to be photoperiod- and age-dependent. However, the differences in its activity were seen only in case of mature tissue. In immature bank voles, reared in both regimes of light aromatase activity was low, while in mature animals a 50% increase was observed. Thus, aromatase activity and estradiol biosynthesis were much lower in the Leydig cell culture from a short day than in the analogus culture fom a long one. The present study also showed different sensitivity to the stimulation of LH between young and adult bank voles kept in different regimes of light, which could be connected with the number of Leydig cells' LH receptors.

Age Factors↗

Effect of the increase of steroid binding plasma levels after passive immunization against testosterone on the control of luteinizing hormone (LH) secretion in ovariectomized underfed dairy heifers.

The ability of passive immunization against testosterone to increase sex steroid binding levels in plasma and thus to overcome the negative feedback of oestradiol-17 beta (E2) on LH secretion in underfed heifers was investigated. Dairy heifers were ovariectomized and divided in 3 groups: high energy diet (H group, n = 4), low energy diet (L group, n = 3) and low energy diet + E2 implants (LE2 group, n = 4). Twenty-four h before injection of bovine immunoglobulins, the mean concentrations of LH were not different between H and L groups. LH baseline was lower (0.8 vs 1.1 ng/ml, P less than 0.03) and the median number of LH pulses was higher (10 vs 5, P less than 0.03) in H than in L group. E2 markedly decreased (P less than 0.01) the mean and basal concentrations of LH (0.27 ng/ml), and number of LH pulses (0) in the LE2 group (P less than 0.05). After injection of anti-testosterone immunoglobulins in the L group, mean and basal LH concentrations tended to decrease. The median number of LH pulses in the L group rose 8 days after immunization (5 vs 7 on day -1 and day +8, P less than or equal to 0.05). Amplitude of pulses tended to decrease after injection (P = 0.08). In the LE2 group, the mean concentration and baseline of LH were not affected by passive immunization against testosterone, while pulses of LH appeared at day +1 and rose (P = 0.07) at day +8 after immunization with 3.5 pulses.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗