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 1,207 records · Page 67Linked to original sources
PubMed1996

[Precocious maturation of the testis associated with excessive secretion of estradiol and testosterone by Leydig cells].

We present the quantitative description of spermatogenesis in a 4.5-year-old boy with precocious puberty, where Leydig cell hyperplasia was associated with excessive secretion of testosterone (T), but predominantly with estradiol (E). The results were compared with data obtained from an age-matched group and adult men without hormonal abnormalities. We showed, that excessive secretion of T and E with relative deficiency of FSH is sufficient to induce testicular tubule maturation and qualitatively complete spermatogenesis, although with a poorer quantitative aspect.

Child, Preschool↗
PubMed1992

Luteinizing hormone differentially regulates the secretion of testicular oxytocin and testosterone by purified adult rat Leydig cells in vitro.

The aims of the present study were to determine whether Leydig cells in vitro synthesize oxytocin, and whether LH modulates the secretion of oxytocin by Leydig cells. Highly purified adult Leydig cells were prepared from adult rats and cultured for 3 days in the presence or absence of 0.1 ng/ml ovine LH, and media were changed daily. The total amount of oxytocin present in the culture was estimated by RIA of cell extracts before culture (day 0) and at the end of day 3 of culture and in media on days 1-3. The content of immunoreactive oxytocin in cell extracts on day 0 (3.4 +/- 1.2 pg/10(6) cells) was significantly lower than the total amount that had been released into the medium and was present in the cell extracts at the end of day 3 (+LH, 27.8 +/- 3.3; -LH, 16.5 +/- 2.7 pg/10(6) cells), suggesting that Leydig cells are able to synthesize and secrete oxytocin. This hypothesis was supported by the observation that oxytocin release into the medium was significantly reduced during a 3-h treatment of Leydig cells with the protein synthesis inhibitor cycloheximide (5 micrograms/ml for 3 h). The role of LH in regulating testosterone production by Leydig cells is well defined, but whether LH also regulates oxytocin is unknown. Therefore, the effects of LH on oxytocin and testosterone production by Leydig cells were compared. The production of both hormones was stimulated by increasing doses of LH (0.001-100 ng/ml), but no further rise in oxytocin release could be elicited with amounts of LH greater than 0.1 ng/ml. Testosterone production, however, continued to increase with doses of LH up to 100 ng/ml. Furthermore, the two hormones differed in the rate of their responses to both 3- and 12-h exposures to LH; testosterone secretion increased more rapidly than that of oxytocin. These data provide direct evidence that adult Leydig cells produce immunoreactive oxytocin, and that their production of this peptide is regulated by LH.

Animals↗
PubMed1995

Parallel nocturnal secretion of melatonin and testosterone in the plasma of normal men.

Differences and similarities in the temporal organization of hormone secretion in plasma reflect the activity of CNS pacemakers. One aspect of this activity, the temporal synchronization of the secretion of different hormones is still poorly understood. We report the analysis of melatonin and testosterone plasma concentrations during two nights in 6 normal healthy young men. Blood was collected every 20 min between 2040 and 0640. Plasma testosterone concentrations increased by 1.5- to 2-fold during the second part of the night, and melatonin by 2.5- to 4-fold. In each subject, the individual temporal pattern of melatonin was quite stable over the two nights of sampling, while testosterone profiles showed fluctuations. There was a high degree of parallelism in these two hormones nocturnal secretion. These results, together with previous studies, suggest that melatonin might entrain the nocturnal secretion of testosterone.

Activity Cycles↗
PubMed1988

Antihormonal activities of 5 alpha-reductase and aromatase inhibitors.

The problem of developing androgen antagonists has been tackled so far only by synthesizing steroids able to displace testosterone and other androgens from their specific receptor sites. The observation that testosterone has to be converted intracellularly either to 5 alpha-reduced metabolites (DHT, 3 alpha-diol, etc.) or to estrogens, in order to become fully active on androgen-dependent structures (both central and peripheral), has opened the possibility of creating molecules which prevent these conversions, and which could then block the actions of testosterone. The availability of these new compounds has allowed a better understanding of the selective physiological role of each of the metabolites of testosterone, and to provide the basis for the development of new hormone antagonists to be used in those clinical conditions for which an inhibition of the actions of testosterone is foreseen. The usefulness of these enzyme inhibitors is underlined by some examples described in this paper. The results obtained may permit the formulation of the following conclusions: (1) The conversion of testosterone to its 5 alpha-reduced metabolites occurring in the neuroendocrine structures may represent an essential step for the appearance of the inhibitory feedback effect testosterone exerts on LH secretion; (2) Testosterone exhibits its negative feedback effect on FSH secretion as such and not following the local aromatization to estrogens; (3) Testosterone exerts its effect on the intrahypothalamic stores of LHRH acting as such and not following its local conversion either to 5 alpha-reduced metabolites or to estrogenic molecules; (4) Some of the new enzyme inhibitors (e.g. 4-OH-A) may represent an interesting tool for the treatment and/or the prevention of BPH and possibly of other androgen-dependent diseases (prostate carcinoma, acne etc.), as shown by their ability to prevent the in vitro conversion of testosterone to its 5 alpha-reduced metabolites both in the normal prostate of the rat and in the human BPH tissue.

Animals↗
PubMedDate not supplied

Mechanism of LHRH-stimulated steroidogenesis in rat Leydig cells: lipoxygenase products of arachidonic acid may not be involved.

Luteinizing hormone releasing hormone agonist, [(imBzl)-DHis6,Pro9,NEt]-LHRH (LHRH-A), caused a two to threefold increase in in vitro testosterone (T) secretion by rat Leydig cells. This LHRH-A-induced T secretion was completely blocked by quinacrine and chloroquine, inhibitors of phospholipase A2. Addition of phospholipase A2, however, was ineffective in stimulating basal or LHRH-A-induced T secretion. Phospholipase C, on the other hand, significantly stimulated both basal and LHRH-A-induced T secretion. Exogenously added arachidonic acid stimulated basal T secretion in a dose dependent manner, the maximum increase being about 100% over basal at a dose of 100 microM. Higher doses of arachidonic acid had no stimulatory effect. In the presence of LHRH-A, the stimulatory effect of arachidonic acid was additive up to a concentration of 100 microM; but higher concentrations of arachidonic acid (200 microM) were inhibitory. LHRH-A-induced steroidogenesis was inhibited by 5, 8, 11, 14 Eicosatetraynoic acid (ETYA), an inhibitor of all the three known pathways of arachidonic acid metabolism, and by nordihydroguaiaretic acid, and inhibitory of the lipoxygenase pathway of arachidonic acid metabolism. LHRH-A-stimulated T secretion was not inhibited by indomethacin, an inhibitor of the cyclo-oxygenase pathway of arachidonic acid metabolism. ETYA inhibited arachidonic acid-induced T secretion. Nordihydroguaiaretic acid, on the other hand, augmented basal, arachidonic acid-, phospholipase C-, or phorbol 12, myristate 13 acetate-induced testosterone secretion. These results suggest that arachidonic acid, whose release is influenced by phospholipase C, is involved in LHRH-A-induced T secretion by rat Leydig cells.(ABSTRACT TRUNCATED AT 250 WORDS)

5,8,11,14-Eicosatetraynoic Acid↗
PubMed1987

Testosterone selectively increases serum follicle-stimulating hormonal (FSH) but not luteinizing hormone (LH) in gonadotropin-releasing hormone antagonist-treated male rats: evidence for differential regulation of LH and FSH secretion.

Both testosterone (T) and gonadotropin-releasing hormone (GnRH)-antagonist (GnRH-A) when given alone lower serum luteinizing hormone (LH) and follicle-stimulating hormone (FSH) in intact and castrated rats. However, when graded doses of testosterone enanthate (T.E.) were given to GnRH-A-treated intact male rats, a paradoxical dose-dependent increase in serum FSH occurred; whereas serum LH remained suppressed. This surprising finding led us to ask whether the paradoxical increase in serum FSH in GnRH-A-suppressed animals was a direct stimulatory effect of T on the hypothalamic-pituitary axis or the result of a T effect on a testicular regulator of FSH. To test these hypotheses, we treated adult male castrated rats with GnRH-A and graded doses of T.E. In both intact and castrated rats, serum LH remained undetectable in GnRH-A-treated rats with or without T.E. However, addition of T.E. to GnRH-A led to a dose-dependent increase in serum FSH in castrated animals as well, thus pointing against mediation by a selective testicular regulator of FSH. These data provide evidence that pituitary LH and FSH responses may be differentially regulated under certain conditions. When the action of GnRH is blocked (such as in GnRH-A-treated animals), T directly and selectively increases pituitary FSH secretion.

Animals↗
PubMed1990

Cell-cell interactions in the control of spermatogenesis as studied using Leydig cell destruction and testosterone replacement.

This review centers around studies which have used ethane dimethane sulphonate (EDS) selectively to destroy all of the Leydig cells in the adult rat testis. With additional manipulations such as testosterone replacement and/or experimental induction of severe seminiferous tubule damage in EDS-injected rats, the following questions have been addressed: 1) What are the roles and relative importance of testosterone and other non-androgenic Leydig cell products in normal spermatogenesis and testicular function in general? 2) What are the factors controlling Leydig cell proliferation and maturation? 3) Is it the Leydig cells or the seminiferous tubules (or both) which control the testicular vasculature? The findings emphasize that in the normal adult rat testis there is a complex interaction between the Leydig cells, the Sertoli (and/or peritubular) cells, the germ cells, and the vasculature, and that testosterone, but not other Leydig cell products, plays a central role in many of these interactions. The Leydig cells drive spermatogenesis via the secretion of testosterone which acts on the Sertoli and/or peritubular cells to create an environment which enables normal progression of germ cells through stage VII of the spermatogenic cycle. In addition, testosterone is involved in the control of the vasculature, and hence the formation of testicular interstitial fluid, presumably again via effects on the Sertoli and/or peritubular cells. When Leydig cells regenerate and mature after their destruction by EDS, it can be shown that both the rate and the location of regenerating Leydig cells is determined by an interplay between endocrine (LH and perhaps FSH) and paracrine factors; the latter emanate from the seminiferous tubules and are determined by the germ cell complement. Taken together with other data on the paracrine control of Leydig cell testosterone secretion by the seminiferous tubules, these findings demonstrate that the functions of all of the cell types in the testis are interwoven in a highly organized manner. This has considerable implications with regard to the concentration of research effort on in vitro studies of the testis, and is discussed together with the need for a multidisciplinary approach if the complex control of spermatogenesis is ever to be properly understood.

Animals↗
PubMed1989

Testosterone administration inhibits gonadotropin secretion by an effect directly on the human pituitary.

Testosterone (T) administration slows LH pulse frequency in man, presumably by an effect on the hypothalamic GnRH pulse generator, but it also may have a direct action on the pituitary. To determine if T does indeed affect gonadotropin secretion by acting directly on the pituitary, we studied the effect of T on GnRH-stimulated gonadotropin secretion. Six men with hypogonadotropic hypogonadism were treated with physiological doses of GnRH (5 micrograms every 2 h, sc by automatic infusion pump) for 6 weeks. Once their gonadotropin levels were normal, the men received a supraphysiological dosage of T enanthate (200 mg, im, weekly for 8 weeks) in addition to GnRH. They then received GnRH alone for a final 8-week period. Blood sampling was performed every 10 min for 8 h at the end of each of the three study periods. T administration suppressed the mean serum LH level to about 50% of the value during GnRH alone [18 +/- 2 (+/- SE) vs. 37 +/- 2 micrograms/L; P less than 0.05] and suppressed the mean serum FSH level to about 30% of the value during GnRH alone (39 +/- 6 vs. 128 +/- 28 micrograms/L; P less than 0.05). Eight weeks after stopping T, while continuing GnRH alone, serum LH and FSH levels were similar to those at the end of the first period of GnRH administration. The mean LH response to GnRH was reduced during T administration (17 +/- 3 micrograms/L) compared to that during the initial period of GnRH alone (31 +/- 4 micrograms/L; P less than 0.05). Serum T and estradiol levels were in the low normal range after GnRH alone before T administration (11 +/- 2 nmol/L and 105 +/- 17 pmol/L, respectively) and increased to just above the normal adult ranges after 8 weeks of T administration (36 +/- 5 nmol/L and 264 +/- 49 pmol/L, respectively). These results demonstrate that T and/or its metabolites inhibit LH and FSH secretion by a GnRH-independent mechanism, probably directly on the pituitary gland, in man.

Adult↗
PubMed1979

Evidence that testosterone can suppress pituitary gonadotropin secretion independently of peripheral aromatization.

Testosterone (T) was given to normal men with and without the concomitant administration of the aromatase inhibitor, delta 1-testolactone (Teslac), to examine the role of peripheral aromatization of T in gonadotropin regulation. When T was administered alone by continuous iv infusion (15 mg/day for 4 days), serum T increased 3-fold (P less than 0.01) and estradiol (E) increased by 50% (P less than 0.01). These changes were associated with a 50% decrease in serum LH and FSH concentrations (P less than 0.01). When T was infused into men taking Teslac (2000 mg/day), serum T levels doubled (P less than 0.01), but E levels did not change (13.4 +/- 1.5 vs. 13.5 +/- 1.0 pg/ml; P = NS). This pattern of plasma steroids, increased T and unchanged E, was also associated with significantly decreased serum LH and FSH concentrations (14.5 +/- 0.4 vs. 8.0 + 0.4 mIU/ml and 9.9 +/- 2.5 vs. 5.8 +/- 0.1 mIU/ml, respectively; P less than 0.01). These data support the hypothesis that T or one of its metabolites can modulate LH and FSH secretion independently of peripheral aromatization to E.

Adult↗
PubMed1980

Testosterone and 17 beta-oestradiol secretion of the human ovary. II. normal postmenopausal women, postmenopausal women with endometrial hyperplasia and postmenopausal women with adenocarcinoma of the endometrium.

A study of the concentration of testosterone and of 17 beta-estradiol in blood drawn from the ovarian and cutal veins of normal oestrogen-deficient postmenopausal women and of postmenopausal women with signs of oestrogen activity, and the subsequent computation of the ovarian production rates of these two hormones, show that in the latter group of women there is a high ovarian secretion of testosterone. The theory is advanced that this ovarian-secreted testosterone is rapidly converted into 17 beta-oestradiol, and that, by thus increasing the levels of circulating oestrogens, ovarian-secreted testosterone contributes, albeit indirectly, to endometrial hyperplasia and possibly to endometrial carcinoma.

Adenocarcinoma↗
PubMed2001

Effects of ovine LH, GH and prolactin, and testosterone on serum testosterone and estradiol-17 beta levels, and seminal vesicle and testicular activity in the catfish Clarias batrachus (L.).

Intraperitoneal administrations of testosterone (0.5 microgram/g body wt), and ovine LH (1.0 microgram/g body wt), GH (5 micrograms/g body wt) and prolactin (10 micrograms/g body wt) daily for 7 days during early prespawning phase (May) in C. batrachus produced varied effects on seminal vesicle (SVSI) and testicular (GSI) weights and biochemical correlates. Testosterone and LH treatments significantly increased serum testosterone level and concentrations of total proteins, fructose, hexosamines and sialic acid in both seminal vesicles and testis. Serum E2 levels increased significantly only after testosterone treatment. GH treatment increased significantly serum testosterone level and only the concentrations of SV hexosamines and testicular protein. Prolactin, however, significantly lowered serum testosterone level and concentrations of total protein, hexosamines in both SV and testis, and testicular fructose and sialic acid levels. The results show that the stimulating effect of LH and GH on SV and testicular activity is mediated through the increased secretion of testosterone and the inhibitory effect of prolactin by decreased testosterone secretion.

Animals↗
PubMed1987

Olfactory bulbs influence testosterone feedback on gonadotropin secretion in male hamsters on long or short photoperiod.

Previous studies have shown that prepubertal olfactory bulbectomy will prevent the testicular regression associated with short photoperiod in golden hamsters. The gonadal regression which normally occurs in hamsters on short photoperiod is known to be due in part to an increased responsiveness of the reproductive neuroendocrine system to the negative feedback actions of testosterone on LH and FSH secretion. The present study tested whether the olfactory bulbs influence the feedback effects of testosterone on gonadotropin secretion. Twenty-four- to 26-day-old male golden hamsters were either olfactory-bulbectomized (BX) or sham-olfactory-bulbectomized. Eight weeks later, all hamsters were castrated, and one half of each group was placed in LD 10:14 (this was called week-8 of the study), while the other half was returned to long photoperiod (LD 14:10). Eight weeks following castration (week 0 of the study), all animals were implanted with silastic capsules containing 0, 4, 8 or 16 mm of testosterone. All hamsters were bled by cardiac puncture at -8, -4, 0, +2, +4, +6 and +8 weeks. The concentration of LH and FSH in these samples was then determined by RIA. BX completely prevented the negative feedback of testosterone on gonadotropin secretion in hamsters on either long or short photoperiod at all levels of testosterone tested in this study. In addition, there were seemingly steroid-independent effects of BX on gonadotropin levels in the castrated hamsters prior to testosterone replacement at weeks -4 and 0.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Metoclopramide-mediated prolactin secretion in patients with idiopathic hypogonadotropic hypogonadism: effect of testosterone therapy.

The secretion of prolactin (PRL) after intravenous metoclopramide was evaluated in six prepubertal subjects with idiopathic isolated hypogonadotropic hypogonadism before and after repeated testosterone (T) injections. The PRL response to metoclopramide was markedly blunted before T treatment, but both the basal and metoclopramide-stimulated PRL secretion became normal after 4 to 15 months of intramuscular T enanthate, although in three of the subjects, serum T was low at the time of the repeat study. These results confirm that the pituitary lactotrophs are normal in this disorder and suggest that the attenuated response observed in the untreated patients is due to the chronic and persistent exposure of the lactotrophs to an environment low in T. The effect of exogenous T on the lactotrophs persists for several weeks after T is discontinued.

Adolescent↗
PubMedDate not supplied

Effect of estrogen and testosterone on the gastric secretion of rats and conscious rabbits.

Shay rats and conscious rabbits were used to study the effect of sex hormones on gastric secretion. Daily injections of estradiol-di propionate and testosterone-propionate were given separately to each set of animals, while the control animals received solvent alone for the same duration of time. Estrogen inhibited gastric acid output but augmented the mucus secretion as evidenced by increased hexosamine and fucose contents; and testosterone had the reverse effects. The effect of estrogen was more potent that of testosterone. An inverse relationship between gastric acid and mucus secretion has been noted. Peptic activity varied independently of the acid output. These hormones seemed to vary the acid output by modifying the composition of mucus secretion.

Animals↗
PubMed1979

Effects of pinealectomy on the secretion of luteinizing hormone, testosterone and prolactin in rams exposed to various lighting régimes.

Two experiments were carried out to study the effects of controlled lighting régimes on plasma levels of LH were low in all groups of rams, which made the detection of significant effects of any treatment very unlikely. Pinealectomy reduced the effects of changes in the daily photoperiod on the patterns of secretion of testosterone and prolactin. These findings establish the pineal gland as an organ which influences the endocrine responses of rams to photoperiodic stimuli and it is concluded that the pineal gland is probably important as a mediator of seasonal reproductive changes in these animals.

Animals↗
PubMed1994

Effects of nitric oxide-related agents on rat testicular function.

The effects of nitric oxide (NO)-related agents on testicular function were examined in male rats with measurements of serum luteinizing hormone, serum testosterone, testicular interstitial fluid (TIF) testosterone, and TIF volumes. Serum and TIF testosterone levels and luteinizing hormone secretion were significantly decreased by the NO donor, isosorbide dinitrate (ISDN), and the NO synthase (NOS) substrate, L-arginine methyl ester, a source for the endogenous production of NO. The effects of ISDN on TIF volumes were inconsistent, but L-arginine methyl ester decreased TIF formation in a dose-dependent manner. In addition, ISDN dose dependently suppressed testosterone secretion stimulated by human chorionic gonadotropin treatment, suggesting that the effects on testosterone secretion were independent of changes in secretion of the endogenous gonadotropin luteinizing hormone. ISDN, L-arginine methyl ester, and the endogenous NOS substrate L-arginine completely blocked testosterone secretion stimulated by the NOS inhibitor NG-nitro-L-arginine methyl ester (NAME), whereas the relatively inactive NOS substrate, D-arginine, only partially blocked NAME-stimulated testosterone secretion. Hydralazine and nicardipine, two vasodilators that do not exhibit prominent NO-related effects, also blocked basal testosterone secretion and testosterone secretion stimulated by the vasoconstrictor NAME.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Oxidoreductases↗
PubMed1985

Testosterone response of cryptorchid and hypophysectomized rats to human chorionic gonadotrophin (hCG) stimulation.

The testosterone responses to a single injection of hCG (100 i.u.) in hypophysectomized (hypox.), cryptorchid or sham-operated rats were followed over a 5-day period. In sham-operated rats, hCG induced a biphasic rise in serum testosterone, peaks being observed at 2 and 72 h. Reduced testis weights, elevated FSH and LH levels and reduced serum testosterone levels were found after 4 weeks of cryptorchidism, but hCG stimulation resulted in a normal 2 h peak in serum testosterone. However, the secondary rise at 72 h in cryptorchid rats was significantly lower than sham-operated rats. Reduced testis weight and undetectable serum FSH and LH levels together with decreased testosterone levels were found 4 weeks after hypophysectomy. Serum testosterone levels rose 2 h after hCG in comparison to hypox. controls but this peak was significantly reduced compared with sham-operated rats. The second rise in serum testosterone began on day 2, peaking on day 4 at levels comparable to that seen in sham-operated rats after hCG. The in vitro basal and hCG stimulated secretion of testosterone by cryptorchid testes was greater than that secreted by normal rat testes (518.0 +/- 45.9 and 3337.6 +/- 304.1 pmol per testis per 4 h compared with 223.6 +/- 24.9 and 1312.9 +/- 141.4 pmol per testis per 4 h for normal rat testes). In cryptorchid animals a single injection of 100 i.u. hCG resulted in a pattern of in vitro refractoriness similar to normal rats, lasting from 12 h to 2 days, during which testosterone secretion was reduced to near basal levels. The in vitro basal and hCG-stimulated secretion of testosterone by hypox. rat testes was severely diminished compared with normal rat testes. The temporal pattern of in vitro secretion of testosterone from hypox. rat testes mimicked the in vivo serum testosterone pattern seen in these animals. This study demonstrates important differences in the in vivo and in vitro testosterone response to hCG after testicular damage.

Animals↗