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 1,621 records · Page 90Linked to original sources
PubMed1998

Mouse Leydig cell culture on microcarriers.

Culturing cells on microcarriers maximizes the ratio of surface area to culture medium volume. The aim of this study was to show microcarrier culture as a useful tool for improvement of steroidogenic activity in mouse Leydig cells. Freshly isolated cells were grown on Sephadex microcarriers, Cytodex 3, and gelatin beads (gelaspheres) that were uncoated, coated with collagen or coated with fibronectin. The cells were cultured in control or LH-supplemented medium. The effect of LH on testosterone and estradiol secretion was studied with appropriate radioimmunoassays. The activity of hydroxysteroid dehydrogenases (3 beta-HSD, 17 beta-HSD) was evaluated histochemically. Leydig cells growing on microcarriers formed colonies. The strongest response to luteinizing hormone stimulation was observed on gelatin beads coated with fibronectin and collagen. In cells growing on a fibronectin layer, very strong activity of 3 beta-HSD and 17 beta-HSD and an increase in steroid hormone levels were observed. Basal and LH-stimulated testosterone and estradiol secretion were all much higher in the microcarrier than in the monolayer culture system. We conclude that Leydig cells maintain differentiated functions more efficiently on collagen- and fibronectin-coated gelasperes than on Sephadex microcarriers and that uncoated gelaspheres are less efficient than coated ones. Pure gelaspheres are unsuitable for improvement of the hormonal and enzymatic activity of Leydig cells.

3-Hydroxysteroid Dehydrogenases↗
PubMed1980

Role of testosterone and of its metabolites in regulating gonadotrophin secretion in the Japanese quail.

In the Japanese quail gonadal steroids can depress plasma levels of LH and FSH. Since it is now accepted that testosterone metabolites may be metabolized to the tissue-active forms of the hormone, the in-vitro tissue incubation has been combined with steroid replaement therapy in vivo to investigate the physiological roles of various testosterone metabolites as inhibitory feedback agents on gonadtorophin secretion in quail. After the incubation of quail pituitary glands for 3 h with labelled testosterone four metabolites could be identified; androst-4-ene-3,17-dione, 5 beta-dihydrotestosterone (5 beta-DHT), 5 beta-androstane-3 alpha, 17 beta-diol and 5 alpha-DHT. No 5 alpha-androstane-3 alpha, 17 beta-diol was found. Quantitatively, androstenedione was the major metabolite and converison of testosterone to 5 beta-metabolites was significantly greater than to 5 alpha-androgens. Hypothalamic and hyperstriatal tissues converted testosterone than to 5 alpha-androgens. Hypothalamic and hyperstriatal tissues converted testosterone to androstendione, 5 beta-DHT and 5 beta-androstane-3 alpha, 17 beta-diol but not to 5 alpha-DHT or 5 alpha-androstane-3 alpha, 17 beta-diol. Gonadotrophin secretion was studied in castrated quail after chronic s.c. implantation of steroid-containing silicone elastomer capsules or acute injection i.m. of steroid in ethanol: saline. Irrespecive of the route of administration seven androgens, listed in descending order of potency, reduced the increased levels of plasma LH: testosterone: 5 alpha-DHT; androstenedione; 5 alpha-androstane-3, 17-dione; 5 alpha-androstane-3 alpha, 17 beta-diol; 5 alpha-androstan-3 alpha-ol-17-one; 5 alpha-androstan-3 beta-ol-17-one. No changes in levels of plasma LH were observed after the administration of 5 beta-DHT, 5 alpha-androstane-3 beta,17 beta-diol, 5 beta-androstante-3 alpha, 17 beta-diol, 5 beta-androstane-3, 17-dione, androst-5-ene-3 beta, 17 beta-diol or androst-5-en-3 beta-ol-17-one. Testosterone and oestradiol-17 beta were effective in inhibiting secretion of both LH and FSH in young photostimulated quail and completely blocked testicular growth: 5 alpha-DHT inhibited only the release of LH and testicular growth was unaffected.

Androgens↗
PubMed1984

Effect of immunoneutralization of LH releasing hormone on LH, FSH and ovarian steroid secretion in the preovulatory phase of the oestrous cycle in the ewe.

Immunoneutralization of LH releasing hormone (LHRH) by the i.v. administration of LHRH antiserum in the preovulatory period in the ewe resulted in a prompt abolition of the pulsatile secretion of LH without alteration of basal plasma levels of LH. This resulted in an immediate cessation of the pulsatile secretion of ovarian oestradiol, with no change in the secretion rate of androstenedione or plasma levels of FSH. The ovarian secretion rate of testosterone increased significantly. Twenty to 22h after the injection of LHRH antiserum, pulsatile secretion of LH and ovarian oestradiol and androgen secretion remained suppressed while plasma levels of FSH had increased significantly. The bolus injection of ovine LH (10 micrograms, i.v.) at this time caused a significant increase in oestradiol, androstenedione and testosterone, these responses being inversely related to the titre of LHRH antiserum in the plasma at this time. These results show that (1) the secretion of oestradiol from the preovulatory sheep follicle is entirely dependent on the pulsatile secretion of LH and (2) since the secretion of ovarian androgens was not inhibited, LH may exert a short-term control over the aromatase enzyme system controlling the conversion of androgen to oestrogen in the granulosa cell of the preovulatory sheep follicle.

Androstenedione↗
PubMed1985

Testosterone administration to ovariectomized female rhesus monkeys (Macaca mulatta) reduces the frequency of pulsatile luteinizing hormone secretion.

In the male rhesus monkey testosterone (T) retards the frequency of intermittent LH secretion. The purpose of the present study was to determine whether this action of T is demonstrable in the female. Five ovariectomized rhesus monkeys, bearing indwelling cardiac catheters, were implanted s.c. on one or more occasions with T-containing Silastic capsules. Sequential blood samples were collected for 8 h every 10 min before T treatment and usually at 1, 2, 4, and 8 days thereafter. Plasma LH concentrations were measured in duplicate by radioimmunoassay and subsequently analyzed with a computerized algorithm. Sustained increments in circulating T (5-13 ng/ml) in ovariectomized monkeys resulted in a progressive reduction in LH pulse frequencies from approximately 1 pulse every 60 min before initiation of T treatment to 1 pulse every 100-150 min at 48 h thereafter. In most cases the deceleration in pulsatile gonadotropin secretion continued, and by 4-8 days of T treatment LH pulse frequencies as low as 1 pulse every 5 h were observed. The onset of the T-induced deceleration in LH pulse frequency was generally associated with an increase in LH pulse amplitude and with a decline in mean LH levels. This LH response in the female to T treatment was similar to that previously reported for male castrates.

Animals↗
PubMed1997

Effects of leuprolide-induced hypogonadism and testosterone replacement on sleep, melatonin, and prolactin secretion in men.

The possible role of gonadal steroids in regulating sleep and circadian rhythms in humans has received relatively little attention despite the importance of the topic to several clinical syndromes. Pharmacologically induced hypogonadism, with and without gonadal steroid replacement, provides an opportunity to examine these questions within a controlled experimental design. We used leuprolide acetate, with and without testosterone replacement, to study the role of testosterone in the regulation of sleep and of melatonin, PRL, and TSH secretion in men. Results from 10 men revealed significant decreases in 24-h PRL levels and in the percentage and time of stage 4 sleep in the hypogonadal state compared with testosterone replacement. There were no differences in melatonin or TSH secretion or in the timing or duration of sleep between the two hormonal conditions. These results indicate that testosterone has relatively specific and discrete effects on sleep and hormonal rhythms in men.

Adolescent↗
PubMed1998

Absence of an inhibitory vasopressinergic tone on LH release in pubertal male rhesus macaques.

During puberty, primates begin to secrete LH, and presumably GnRH, at night and then eventually throughout the day as they mature. We examined the role of vasopressin, a putative inhibitor of the GnRH pulse generator, on LH secretion in pubertal male macaques both during the day when the GnRH pulse generator was not active and during the night when pulsatile LH secretion was observed. As has been found in other primates, LH and testosterone levels were low during the day and elevated at night. A potent vasopressin receptor antagonist (VPa) was administered during the middle 5 h of a 15-hour daytime or nighttime blood collection period to determine the effects on LH, testosterone and cortisol secretion. Both during the day and night, cortisol secretion was elevated during VPa infusion, suggesting that this V1a receptor antagonist has agonist activity on the V1b receptor in the pituitary involved in vasopressin-stimulated corticotropin release. Mean LH levels during VPa infusion were not different from the control period for that group during the day when LH secretion was absent. Mean LH levels were significantly higher (p < 0.05) than pre-VPa LH levels at night when pulsatile LH secretion was observed. However, LH levels at night during VPa were not higher than levels in untreated animals at the same time. The results of these studies demonstrate that LH and testosterone profiles are similar to those observed in human males during the pubertal transition and suggest that the absence of daytime gonadotropin release during puberty is not due to inhibitory vasopressinergic tone on the GnRH pulse generator.

Animals↗
PubMed2000

Testicular dysfunction in men with primary hypothyroidism; reversal of hypogonadotrophic hypogonadism with replacement thyroxine.

OBJECTIVE: Primary hypothyroidism can cause disturbances in normal gonadal function. The aim of this study was to investigate the relationship in men between hypogonadism and primary hypothyroidism and the extent to which free and total testosterone levels rose after introduction of replacement thyroxine. DESIGN: Paired study of patients in a hypothyroid and thyroxine treated state. PATIENTS: Ten men with primary hypothyroidism. MEASUREMENTS: Free and total testosterone, gonadotrophin and prolactin levels before and after thyroxine replacement therapy. RESULTS: Low free testosterone levels (161 +/- 62 pmol/l) demonstrated at the time the men were hypothyroid rose significantly with the commencement of thyroxine replacement (315 +/- 141 pmol/l; P < 0.001). Gonadotrophin levels were not elevated consistent with hypogonadotrophic hypogonadism. Hyperprolactinaemia, which can occur in primary hypothyroidism and cause hypogonadotrophic hypogonadism, was not present in the majority of these patients. However a reduction in prolactin level was evident with thyroxine replacement and a rise in free testosterone levels. CONCLUSION: This suggests an effect of hypothyroidism on gonadotrophin secretion at the level of the hypothalamus-pituitary, either directly or through modulation of prolactin secretion. Low free testosterone may also be a contributing factor to some of the symptoms and signs of hypothyroidism in men.

Adult↗
PubMed1997

Ethanol, growth hormone and testosterone in peripubertal rats.

The deleterious effects of ethanol on the hypothalamic pituitary growth hormone axis in adult male humans and animals have been well documented. It is also well established that ethanol has toxic effects on testicular function in adult humans and animals. Much less is known, however, about the effects of ethanol on the growth hormone (GH) axis and testicular function in adolescence. Recent studies have established that adolescent problem drinking is a widespread and growing threat to the health of young people in the United States. In the present study, therefore, we investigated if acute ethanol exposure in peripubertal male Sprague-Dawley rats altered normal pituitary and testicular function. Serum levels of GH and testosterone were measured at 1.5, 3, 6, and 24 h after a single i.p. injection of either saline or 3 g/kg body weight ethanol. Histologic analysis as well as serum testosterone levels allowed us to assign animals to either early puberty (35-day-old animals), mid-puberty (41-day-old animals), or young adult (51- and 66-day-old animals) status. Ethanol produced significant decrements in serum testosterone in the 51- and 66-day-old animals, with a trend toward suppression in the 41-day-old group. Furthermore acute ethanol administration significantly decreased serum GH (P < 0.0001 by 3 way ANOVA) demonstrating a significant effect of ethanol on serum GH in all age groups and at all time points studied when compared with saline injected controls (P < 0.01 by Turkey's studentized range test). Despite this significant fall in peripheral GH levels, there was no decrease in either GH mRNA or growth hormone-releasing factor (GRF) mRNA levels nor in hypothalamic concentration of GRF peptide. We conclude that, as in adult animals, acute exposure to ethanol causes a prolonged and severe decrement in serum GH which is possibly mediated at the level of secretion. In addition, there is attenuation in testosterone secretion. These data are all the more important since GH and testosterone play critical roles in organ maturation during this stage of development.

Analysis of Variance↗
PubMedDate not supplied

Regulation of testosterone production in the adjuvant-induced arthritic rat.

Serum testosterone concentrations are reduced in men with rheumatoid arthritis and in rats with adjuvant-induced arthritis, a common model for rheumatoid arthritis. To understand the mechanism responsible for this reduction, testosterone production by testicular cells and Percoll-purified Leydig cells from nonarthritic and arthritic rats was studied. Leydig cells in crude interstitial cell preparations from arthritic rats secreted significantly less testosterone in response to human chorionic gonadotropin (hCG) stimulation than cells from nonarthritic animals. In contrast, no differences in hCG and dibutyryl cyclic adenosine monophosphate-stimulated testosterone production by Percoll-enriched Leydig cells from arthritic and nonarthritic animals were observed. To determine whether a secretory product from testicular macrophages was important to this reduction, macrophages from arthritic and nonarthritic animals were cultured. The conditioned media from these cultures were added to cultures of interstitial cells from nonarthritic animals. Nonarthritic rat testicular macrophage-conditioned medium had no significant effect on testosterone production. In contrast, conditioned medium from arthritic rat testicular macrophages significantly reduced testosterone production. These results suggest that testicular macrophages secrete a factor that may be important in the regulation of testosterone production in the adjuvant-induced arthritic rat.

Animals↗
PubMed2004

Testosterone blunts feedback inhibition of growth hormone secretion by experimentally elevated insulin-like growth factor-I concentrations.

The present study tests the hypothesis that a high dose of testosterone (Te) drives GH and IGF-I production, in part, by blunting autonegative feedback by the end-product peptide. To this end, we infused saline or recombinant human IGF-I (10 microg/kg.h iv for 6 h) in seven healthy men ages 51-72 yr after administration of placebo (Pl) and Te in randomized order. GH release was quantitated fasting before and after injection of GHRH (1 microg/kg). Statistical analyses disclosed that Te vs. Pl: 1) increased the mean concentration of GH from 0.15 +/- 0.045 to 0.48 +/- 0.11 microg/liter (P = 0.007) and IGF-I from 108 +/- 5.0 to 124 +/- 4.1 (P = 0.047) without altering GHRH-induced GH release; 2) elevated the GH nadir from 0.13 +/- 0.03 to 0.23 +/- 0.06 microg/liter (P < 0.05) in the control session and from 0.06 +/- 0.02 to 0.14 +/- 0.04 microg/liter (P = 0.038) during IGF-I infusion; 3) augmented GHRH-stimulated GH release from 3.0 +/- 0.56 (Pl) to 3.7 +/- 0.52 microg/liter (Te) (P < 0.05) during IGF-I infusion; and 4) did not influence estimated IGF-I kinetics. In summary, supplementation of a high dose of Te in middle-aged and older men attenuates IGF-I feedback-dependent inhibition of nadir and peak GH secretion. Both effects of Te differ from those reported recently for estradiol in postmenopausal women. Accordingly, we postulate that Te and estrogen modulate IGF-I negative feedback differentially.

Aged↗
PubMed2006

Responses of the steroid circadian system to alcohol in humans: Importance of the time and duration of intake.

Reports provide conflicting data about the effects of alcohol consumption on the hormonal system. Any study of these effects must control for a number of variables, including sex, alcohol status (alcoholic addiction vs. non-addiction), medical status (malnutrition, liver disease), and conditions of alcohol exposure, including an acute or continuous pattern of intake. The latter appears to be an especially critical factor in interpreting these effects. The authors therefore conducted a trial with a circadian design in which alcohol was administered repeatedly and regularly over a 26 h period for a total dose of 256 g. Because this protocol involves continuous alcohol administration, it is similar to administration among alcoholics and thus sheds new light on alcohol's effect on hormone secretion. Using healthy volunteers rather than alcoholics, however, prevents any confounding due to liver disorders and nutritional deficiencies, and thus makes it possible to focus on the direct role of alcohol in hormonal modifications. In these conditions, the continuous administration of alcohol did not affect cortisol secretion, but serum testosterone levels were significantly higher at all time points during the alcohol session than at the corresponding time points during the control session. These data are not consistent with previously reported findings for the relation between alcohol and both cortisol and testosterone, because in the current experiment the action of ethanol on steroid secretion should involve the circadian clock more than the hormonal system itself.

Adolescent↗
PubMed1998

In vitro action of testosterone in potentiating gonadotropin-releasing hormone-stimulated gonadotropin-II secretion in goldfish pituitary cells: involvement of protein kinase C, calcium, and testosterone metabolites.

Overnight preincubation of goldfish pituitary cell culture with testosterone (T) enhanced the gonadotropin (GTH)-II responses to GTH-releasing hormone (GnRH). In this study, the involvement of GnRH signal transduction components and the requirement for T metabolism in mediating this direct, pituitary cell action of T were examined using cultured pituitary cells from both male and female goldfish. Each sets of related experiments were done in at least two different stages of the gonadal reproductive cycle and similar effects were observed. Overnight treatment with 10 nM T increased GTH-II responses to maximal stimulatory doses (100 nM) of either salmon (s)GnRH or chicken (c)GnRH-II, but not the total cellular GTH-II contents measured prior to and after a 2-h GnRH challenge. T increased the efficacy and sensitivity of the GTH-II response to stimulation by a protein kinase C (PKC) activator, tetradecanoyl phorbol acetate (TPA) without altering the ED50 of the dose-response curve. In T-treated cells, addition of a PKC inhibitor attenuated GTH-II responses to 100 nM doses of sGnRH, cGnRH-II, or TPA. T did not affect the GTH-II release stimulated by high concentrations of the Ca2+ ionophore ionomycin (100 microM) and the voltage-sensitive Ca2+ channel (VSCC) agonist Bay K 8644 (10 microM); similarly, the sensitivity of the GTH-II response to ionomycin and Bay K 8644 was also unaltered. Taken together, these data suggest that T potentiates GnRH-stimulated GTH-II release by enhancing the effectiveness of PKC-dependent pathways, but not by increasing the total Ca2+-sensitive GTH-II pool, the sensitivity of the release response to increases in intracellular Ca2+, or the amount of available GTH-II. However, the VSCC agonist nifedipine reduced sGnRH- and cGnRH-II-elicited GTH-II release in T-treated as well as in non-T-treated cells, suggesting that VSCC dependence is still present in the GnRH-induced response following exposure to T. Since total cGnRH-II binding to pituitary cells was not increased by T, increases in GnRH receptor capacity are unlikely following T treatment. The ability of T to increase GnRH-stimulated GTH-II secretion was not mimicked by 11-ketotestosterone or dihydrotestosterone, but was abolished by coincubation with an aromatase inhibitor. When viewed together, these observations suggest that aromatization of T may be required for the pituitary action of T on GnRH-induced GTH-II release.

Animals↗
PubMed1987

Stimulation of calcitonin secretory capacity by increased serum levels of testosterone in men treated with tamoxifen.

Previous studies have suggested that sex steroids, including both oestrogen and testosterone, influence calcitonin secretion. However, a negative effect of gonadotrophins on calcitonin has not been excluded. Twelve men with infertility and low-normal serum levels of testosterone were studied before and during tamoxifen therapy. Increases in the serum levels of LH, FSH, testosterone and calcitonin were observed after treatment. Our findings suggest that testosterone has a direct influence on calcitonin secretion.

Calcitonin↗
PubMed1990

Modulatory effect of testosterone on the serotoninergic control of prolactin secretion in prepubertal rats.

The administration of 5-hydroxytryptophan (5-HTP) induced a prolactin release in male and female prepubertal rats at 20 days of age. This response was significantly higher in male than in female rats. Neonatal androgenization of the females significantly increased the release of prolactin induced by 5-HTP treatment compared to the values observed in males; thus, the neonatal exposure to androgens seems to be responsible for the sexual differences in the prolactin response to 5-HTP. In a second series of experiments the effect of this serotoninergic precursor on prolactin release in prepubertal (16, 26, and 30 days of age), peripubertal (45-day-old) and adult male rats was studied. Castration significantly decreased the prolactin release response to 5-HTP in prepubertal rats. The administration of testosterone to castrated rats markedly increased the prolactin release response to 5-HTP. Neither castration nor testosterone administration modified the prolactin response to 5-HTP in peripubertal and adult rats. These results appear to indicate that testosterone modulates the serotoninergic control of prolactin secretion during the prepubertal stage. The control of prolactin levels could be one of the mechanisms by which testosterone participates in the sexual maturation.

5-Hydroxytryptophan↗
PubMed1978

Effects of 15(S)-15-methyl prostaglandin F2 alpha methyl ester-containing silastic discs in male rats.

Silicone rubber discs containing 15(S)-15-methyl prostaglandin F2 alpha ester (15-Me-PGF2 alpha) in the matrix were implanted in the left side of the scrotums of Sprague-Dawley rats. The effect of 1% and 2% drug concentration was examined for 10, 20, or 28 days and compared with the effects of Silastic discs containing no prostaglandin. The discs containing prostaglandin reduced mean testicular and accessory gland weights. Histologically the testes and epididymides showed decreased or absent spermatogenic elements and hypertrophy of the interstitial cell masses in comparison with other cells. Implanted prostaglandin significantly depressed serum testosterone, luteinizing hormone, and follicle-stimulating hormone (FSH) concentrations when 15-Me-PGF2 alpha plasma concentrations exceeded 2 ng/ml. Hormone concentrations returned to control values as drug concentrations declined. FSH concentrations significantly exceeded control values 10 and 20 days after implantation, when prostaglandin concentration was nondetectable. The acute suppression of all three hormones suggest that 15-Me-PGF2 alpha either may act directly on the tests to suppress testosterone production or may suppress testosterone production or may suppress gonadotropin secretion, resulting in depressed testosterone output.

Animals↗
PubMed1989

Luteinizing hormone response to an oestradiol challenge in 5 intersex pigs possessing ovotestes.

After challenge with oestradiol benzoate, the mean maximum LH concentration in 5 XX intersex pigs possessing ovarian and testicular tissue, or only testicular tissue, was 2.10 (+/- 0.41) ng/ml compared with 8.9 ng/ml in mature domestic gilts. These results indicate that exposure of the pig brain to testosterone before Day 30 of gestation is important, or that early testicular secretions other than testosterone are involved in the determination of brain gender. The observation that some intersex pigs show normal oestrous cycles implies that the response to these prenatal factors is primarily quantitative rather than qualitative.

Animals↗
PubMed1986

Neuroendocrine changes characteristic of sexual maturation.

A general scheme of neuroendocrine factors influencing the onset of puberty is presented. Gonadotropin-releasing hormone (GnRH) is secreted in pulsatile fashion by the arcuate nucleus of the hypothalamus. Amplitude and probably frequency of the secretory pulses of GnRH increase at the time of puberty, stimulating the secretion of pituitary gonadotropins (LH and FSH). In turn, the gonadotropins induce the maturation of the ovarian follicles in the girls, spermatogenesis in the boys, and the secretion of estradiol or testosterone. The increase of the pulsatile secretion of GnRH is sufficient for explaining the onset of puberty. The response of the pituitary gonadotropins to GnRH would depend on the presence of sex steroids through the feedback mechanisms. The secretion of GnRH may be influenced by neurotransmitters. Norepinephrine, epinephrine and dopamine would stimulate GnRH secretion. Such effect, in fact, depends on the steroid milieu. Opposite effects can be observed in absence of estradiol. Serotonin has a negative effect on the GnRH secretion. Melatonin appears also to block GnRH secretion at the time of puberty. Finally, beta-endorphins decrease the frequency of GnRH secretion only in the presence of steroids. It is probable that stress and underweight act in blocking the pubertal development through the action of neurotransmitters, in particular catecholamines and beta-endorphins.

Adolescent↗