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PubMed1998

The follicular endocrine environment in stimulated cycles of women with endometriosis: steroid levels and embryo quality.

OBJECTIVE: To assess the endocrine milieu in follicles of stimulated cycles comparing women with and without endometriosis. Steroids were measured in follicular fluid (FF) and in in vitro culture of granulosa-luteal cells, and this status was related to the quality of the embryos obtained after IVF. DESIGN: Case-control study. SETTING: IVF program at the Instituto Valenciano de Infertilidad. PATIENT(S): Twenty-four women with laparoscopically documented endometriosis and 26 controls undergoing IVF. INTERVENTION(S): Individual follicular aspiration, oocyte isolation, FF storage, and preparation of luteinized granulosa cells for culture; oocyte insemination and embryo cleavage in standard IVF. MAIN OUTCOME MEASURE(S): Serum (day of ovum pickup) and FF measurements of estradiol, progesterone, testosterone, and androstenedione. Secretion of progesterone was measured in the cell-conditioned medium. Results were compared between patients with endometriosis and controls, as well as between oocytes that yielded embryos of different quality. RESULT(S): Levels of progesterone in the FF increased with the severity of the disease, whereas testosterone accumulation in the FF decreased with the severity of the disease. An increase in progesterone accumulation in vitro was observed in basal and hCG-induced granulosa cell cultures. No difference was observed in terms of embryo quality, and no steroid marker was able to identify follicles with oocytes that displayed embryos of good or bad quality under the inverted microscope. CONCLUSION(S): The data show differences in the steroidogenesis of follicles from stimulated women with and without endometriosis. These changes indicate good endocrine health but are not predictive of embryo quality.

Adult↗
PubMed1989

A rat seminiferous epithelial factor that inhibits Leydig cell cAMP and testosterone production: mechanism of action, stage-specific secretion, and partial characterization.

To elucidate further the seminiferous tubule-Leydig cell interaction we studied the effect of spent medium from 20 h rat seminiferous tubule cultures (STCM) on cyclic adenosine monophosphate (cAMP) and testosterone (T) production of Percoll-purified Leydig cells. 8% of STCM inhibited the human chorionic gonadotropin (hCG)-stimulated cAMP production by 30% in a 3 h, and 33% of STCm by 60% in a 20 h incubation. Likewise, a 40% decrease was found in the presence of 8% of STCM in the hCG-stimulated T production in a 3 h incubation. A similar inhibitory activity could be demonstrated in steroid-free rat interstitial fluid. STCM did not affect the viability of the Leydig cells (90-95% after a 20 h incubation) as judged by trypan blue exclusion and the adenosine triphosphate (ATP) content of the cells. Heating (80 degrees C for 10 min) abolished the inhibiting activity, and fractionation with Millipore Ultrafree filters showed that the inhibiting factor had an Mr of 30,000-100,000. When media from different stages of the seminiferous epithelial cycle were analyzed, only stages IX-I showed inhibition of T production (P less than 0.05). The cAMP production inhibiting activity was present in all stages, but stages IX-I showed significantly (P less than 0.05) greater inhibition than stages II-VI. STCM (16%) also inhibited cholera toxin- and forskolin-stimulated cAMP formation (approximately 50 and 60%, respectively; P less than 0.01), and the inhibitory activity persisted after a 3 h preincubation of Leydig cells with 100 micrograms/l pertussis toxin.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Differential responses of hypothalamic LHRH-I and -II to castration and gonadal steroid or tamoxifen treatment in cockerels.

Changes in the hypothalamic contents of LHRH-I and LHRH-II were determined in intact and castrated cockerels injected i.m. with gonadal steroids or tamoxifen. An increase in the plasma concentration of LH after castration was accompained by a significant increase in the content of LHRH-I in the posterior hypothalamus (including the mediobasal hypothalamus and median eminence) which was reversed by oestradiol benzoate given on days 14 and 15 after castration. Under similar circumstances, testosterone propionate did not modify the hypothalamic content of LHRH-I, even though both steroids reduced the plasma concentrations of LH to levels below those of intact cockerels. Treatment of intact cockerels with oestradiol benzoate significantly increased the content of LHRH-I in the posterior hypothalamus, whilst testosterone propionate was again without effect. Tamoxifen significantly raised the plasma concentration of LH in intact cockerels and partially antagonized the suppressive effect of oestradiol benzoate and testosterone on LH secretion in castrated cockerels. However, an anti-oestrogenic effect of tamoxifen on the hypothalamic content of LHRH-I was not demonstrated. There was no evidence of any changes in the hypothalamic content of LHRH-II after castration, with or without gonadal steroid replacement. A change in the hypothalamic content of LHRH-I in response to manipulation of the steroid environment would imply an involvement of this peptide in the mechanism by which gonadal steroids regulate the release of LH. The absence of changes in the hypothalamic content of LHRH-II in the same circumstances suggest that it is not directly involved in the control of LH secretion by the gonadal steroid negative feedback loop.

Animals↗
PubMed1983

Gonadal growth and gonadal hormones do not participate in the development of responsiveness to photoperiod in the golden hamster.

Photoperiod regulates seasonal reproductive cycles in adult golden hamsters but does not influence the timing of puberty in juvenile hamsters. We examined whether pubertal gonadal growth or gonadal hormones were important for the development of photoperiodic responsiveness in hamsters. In one experiment, hamsters raised on long or short days were implanted with 20 mm of testosterone-filled Silastic capsules between 2 and 12 weeks of age. This treatment completely prevented testis growth in 50% of the hamsters on short days and retarded testis growth in hamsters on long days. When the capsules were removed at Week 12, the testes of hamsters on long days matured to adult size within 4 weeks. The testes of hamsters on short days showed no signs of growth for 9 weeks after testosterone was removed whether testis growth had been completely suppressed or only partially suppressed through Week 12. In the second experiment, hamsters born and maintained on long days for 8 weeks were castrated either at 1 week of age or at 8 weeks of age. Half of the animals in each of these groups were exposed to short days from 8 to 19 weeks of age. All hamsters were challenged with various doses of testosterone between 15 and 19 weeks and blood samples were collected after each dose for measurement of luteinizing hormone (LH) and follicle-stimulating hormone (FSH). Hamsters exposed to short days were more sensitive to the negative feedback effects of testosterone on gonadotropin secretion than hamsters on long days, whether castrated as neonates or as adults.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2003

Demonstration of progesterone receptor-mediated gonadotrophin suppression in the human male.

OBJECTIVE: Synthetic gestogens in combination with testosterone have potential as a male hormonal contraceptive, predominantly acting by augmenting suppression of gonadotrophin secretion. Little is known, however, of the effects of gestogens in the male. Gestogens have affinity for both androgen and progesterone receptors but the relative contribution of action at these two receptors in gonadotrophin suppression remains unclear. In this study the effects of progesterone, with no significant androgen-receptor affinity are compared to desogestrel, a synthetic gestogen with relatively low affinity for the androgen receptor, on gonadotrophin secretion in normal men. DESIGN: Subjects received either 50 mg progesterone intramuscularly (i.m.) or 300 micro g desogestrel orally daily for 7 days. Frequent blood sampling over 12 h was undertaken before and after drug administration. GnRH [100 micro g intravenously (i.v.)] was administered 2 h before the end of the frequent sampling period. SUBJECTS: Twenty healthy men were randomly allocated to the two treatment groups. RESULTS: Both progesterone and desogestrel administration resulted in decreases in the concentration of both LH and FSH secretion, as well as testosterone. Analysis of the pulsatile nature of LH secretion indicated that both treatments reduced LH pulse amplitude, and that progesterone reduced LH pulse frequency. Progesterone, but not desogestrel, treatment also reduced the increase in LH secretion in response to GnRH. CONCLUSIONS: The effects of progesterone were at least as marked as those of a maximally effective dose of desogestrel. As progesterone has negligible affinity for the androgen receptor, these results are compatible with the suppressive effects of synthetic 19-norgestogens on gonadotrophin secretion in the male being mediated via the progesterone receptor, with its androgenicity contributing minimally to gonadotrophin suppression.

Administration, Oral↗
PubMed1983

Concentrations of immunoreactive luteinizing hormone releasing hormone in discrete brain regions of the cockerel: effects of castration and testosterone replacement therapy.

The validity of using a radioimmunoassay employing an antiserum raised against synthetic luteinizing hormone releasing hormone (LH-RH) for the quantification of luteinizing hormone releasing factor (LH-RF) in birds was investigated. Extracts of avian hypothalamus yielded displacement curves which were parallel to that of the synthetic LH-RH standard and the immunoreactive potencies of a number of extracts assayed concurrently using two different anti-LH-RH sera were found to be similar. Moreover, after chromatography of cockerel hypothalamic extract on carboxymethyl-cellulose, immunoreactive and biologically active LH-RF were found in the same eluate fractions. Immunoreactive LH-RH was shown to be widely distributed in cockerel hypothalamus with the highest concentrations present in the mediobasal hypothalamus (MBH; 6.55 +/- 1.86 pg/microgram protein, n = 6) and medial preoptic region (POR; 0.95 +/- 0.07 pg/microgram protein, n = 6). The postcastration rise in plasma LH in the cockerel was accompanied by significant (P less than 0.05) increases in the concentration of LH-RH in five hypothalamic areas including the POR; testosterone replacement therapy completely reversed these effects. Although castration raised the mean concentration of LH-RH in four other hypothalamic areas including the MBH, these differences were not significant. However, testosterone replacement therapy depressed LH-RH in all four regions to levels significantly (P less than 0.05) less than those in castrated cockerels. These findings constitute the first direct evidence that the negative feedback action of testosterone on LH secretion in the cockerel is mediated, at least in part, by an action on hypothalamic LH-RF-producing neurones.

Animals↗
PubMed1993

Relationship between gonadotrophins, inhibin and sex steroid secretion during the periovulatory period and the luteal phase in the blue fox (Alopex lagopus).

The blue fox is a monestrous seasonal breeder with a pro-oestrus and oestrus lasting several days and a prolonged luteal phase in non-pregnant as well as pregnant vixens. Ovulation occurs 2 days after the preovulatory luteinizing hormone (LH) peak at the onset of oestrus; oocytes are ovulated as primary oocytes and maturation is completed 2-3 days later. Fertilization is possible during all stages of oocyte maturation until degeneration of oocytes 5 or 6 days after the LH peak. In this study, changes in plasma concentrations of follicle-stimulating hormone (FSH) and immunoreactive inhibin (iINH) and their relationships with LH, oestradiol, androstenedione, testosterone and progesterone secretion and with the periovulatory events, were determined throughout the reproductive cycle of 14 vixens. In late anoestrus and pro-oestrus, FSH and iINH were inversely related to each other (r = -0.84, P < 0.001); whereas FSH concentrations declined to reach low values within the 5 days preceding the LH peak, iINH secretion increased, as did that of oestradiol and androgens. Thereafter, iINH and steroid concentrations with the exception of progesterone reached maximal values at the time of the LH and FSH peaks and decreased within the following 2-3 days in the early luteal phase. Progesterone started to increase simultaneously with the LH peak, and when oocyte maturation was completed (around day 4), progesterone concentrations were increasing, while those of other hormones were low. A postovulatory release of FSH was detected between days 6 and 10; it preceded the rise in iINH, which began on day 8 when concentrations of progesterone were already high and those of oestradiol and LH were low. Progesterone and iINH were positively correlated over the period day 6 to day 49 (r = 0.62, P < 0.01). These results indicate that, in the blue fox, iINH is secreted by the preovulatory follicle and the corpus luteum; that during pro-oestrus, iINH may act in synergy with oestradiol to reduce the secretion of FSH and that after the LH peak the decrease of iINH and oestradiol concentrations may be responsible for the postovulatory release of FSH, which in turn causes an increase in iINH, possibly secreted by the corpus luteum and, as a result, FSH secretion is suppressed.

Androstenedione↗
PubMed2000

Effects of testosterone, FSH, and LH on oestradiol and progesterone secretion by preovulatory cumulus oophorus complexes of the rat.

Female Wistar rats exhibiting a regular 4-day oestrous cycle were included in this study. They were killed in succession on the day of pro-oestrus at 11.00, 18.00, and 22.00 h. From ovarian preovulatory follicles cumulus oophorus complexes (COCs) were isolated and subsequently cultured with or without testosterone (T), T plus FSH, or T plus LH. In control cultures COCs isolated at all investigated hours released similar amounts of oestradiol. T stimulated this basal secretion and the effect was usually enhanced in the presence of FSH or LH. In control cultures the amount of released progesterone was greatest when expanded COCs were isolated (22.00 h). T present in culture media diminished the amount of secreted progesterone. However, when T was added with FSH or LH a distinct stimulatory effect was observed, except in cultures with T plus FSH set up at 22.00 h. Previously, gonadotrophins alone did not effect progesterone secretion. The results suggest that T can regulate steroid, and especially progesterone secretion by COCs. Until the preovulatory gonadotrophin surge T can inhibit luteinization of COCs, while afterwards, acting synergestically with gonadotrphins (especially with LH), T can stimulate progesterone production in the cumulus granulosa cells.

Animals↗
PubMed1988

Immunocytochemical localization of hypothalamic luteinizing hormone-releasing hormone in male ferrets.

LHRH-containing neurons within the hypothalamus were immunocytochemically identified in adult male ferrets that were either gonadally intact, castrated, or castrated and treated with testosterone. The distribution of LHRH-immunopositive neuron cell bodies was similar in the three treatment groups. The majority of these cells was located mediobasally in the retrochiasmatic area, including some within the ventrolateral aspects of the arcuate nucleus. These soma were associated with a dense basal LHRH fiber plexus which extended to the median eminence. A smaller number of cell bodies was found slightly more dorsal and lateral to the major concentration at the base and midline. Isolated LHRH perikarya were occasionally observed in dorsal areas of the hypothalamus. There were no differences in the mean total number of hypothalamic LHRH cell bodies identified in the three treatment groups. These results indicate that the documented negative feedback effects of testosterone on LH secretion in male ferrets are not the result of an alteration in the absolute number of neurons capable of synthesizing LHRH.

Animals↗
PubMed1994

[Neuroendocrinological aspects of aging].

Aging is accompanied by important changes in the production and secretion of hormones. These partly arise from changes in the peripheral endocrine glands themselves but are also partly the consequence of changes in the neuro-endocrine regulating centers of the hormone secretion. Considering e.g. the male gonads, we know that the reduced androgen secretion (and the diminished spermatogenesis) along the ageing process is the consequence of changes in the testes, such as the reduced number of Leydig- and Sertoli-cells, as well as a reduced testicular blood-perfusion. But on the other hand, it should also be partly ascribed to functional changes of the hypothalamohypophysis. This appears from the lowered circadian rhythms of the testosterone levels, the lower plasma levels of free testosterone, although the secretion capacity of the Leydig-cells and the gonadotrophs is maintained. This points to a lower feed-back set-point of the gonadostat. Moreover the amplitude of the LH impulses and the lower opioid tonus are decreased in elderly men. In aged people, the secretion of the adrenal cortex is essentially characterized by an age-related drop of the androgen secretion (DHEAS) and a lower androgens-response to ACTH. This demonstrates changes in the adrenal gland itself. On the other hand, the secretion of cortisol and the production rates of this hormone remain rather stable, although the feedback centre is less sensitive in old lab-animals. This is suggested by a longer lasting and higher cortisol secretion after stress. According to Sapolsky, this is the consequence of a drop in the number of corticoid receptors in the hippocampus, following a loss of neurons, which would be the result of repeated stress. This progressive deterioration of the feed-back locus by the final hormone is also called: "neurohumoral hysteresis". Signs of its existence in aged people can only be found in pathological cases, such as depression or Alzheimer's disease. The secretion of growth hormone, and its plasma levels, as well as their response to "Growth hormone releasing hormone" (GHRH) is severely reduced in old people. This does not appear to be the consequence of the decreased number of somatotropic cells in aged people but seems to be caused by an increased somatostatin secretion by the hypothalamus. It means that this reduced growth hormone secretion has mainly a central origin.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenal Cortex Hormones↗
PubMed2005

The effect of intramuscular injections of boar pheromone 5alpha-androstenol on the hormonal regulation of the estrous cycle in hypoosmatic gilts.

Until 1999 it was accepted that pheromones act exclusively by stimulating the dendritic receptors present in olfactory epithelium. Cycling gilts with an experimentally-disrupted neural olfactory pathway were used to test the hypothesis that boar pheromone 5alpha-androstenol may affect the secretion of hormones involved in the regulation of the estrous cycle by the humoral pathway. On day 12 of the estrous cycle the nasal cavity of gilts (n=15) was irrigated with zink sulfate solution. From day 16 to 20, the experimental group (n=10) was injected intramuscularly with 5alpha-androstenol (20 microg) twice a day. Blood samples were collected from the jugular vein at 4 h intervals on days 17-21 to estimate plasma concentration of LH, oxytocin, estradiol-17beta, testosterone and progesterone. The experimental group displayed a significantly lower mean concentration of LH than the control animals (P<0.0001). The decrease in concentration of LH was accompanied by the reduction of oxytocin (P<0.001), estradiol-17beta (P<0.001) and testosterone (P<0.01) secretion. These results demonstrated that 5alpha-androstenol influenced hormonal regulation by humoral pathway and might be considered to be the priming pheromone in gilts.

Androstenols↗
PubMed1981

Leydig cell tumor with gynecomastia: hormonal effects of an estrogen-producing tumor.

A patient with a testicular interstitial cell tumor and gynecomastia is reported. The testicular tumor was capable of aromatizing 8.3% testosterone. Spermatic venous samples taken from the tumor-bearing side had marked elevations of 17 beta-estradiol (E2), progesterone, and 17-hydroxyprogesterone (170 HP). The progesterone to 17OHP and 17OHP to androstene-dione ratios suggested an enzymatic block of 17 alpha-hydroxylase and 17-20 lyase possibly secondary to locally produced E2. The E2 produced by the tumor appeared to suppress gonadotropin secretion. The plasma testosterone and gonadotropin levels rose within 7 days after the removal of tumor, and the gynecomastia began to decrease.

Adult↗
PubMed1997

Gonadotrophin and prolactin secretion in castrated male sheep following subcutaneous or intracranial treatment with testicular hormones.

Interactions between testosterone, estradiol, and inhibin in the control of gonadotrophin secretion in males are poorly understood. Castrated rams were treated with steroid-free bovine follicular fluid (bFF), testosterone, or estradiol and for 7 d (2 x 2 x 2 factorial design). Given independently, none of the exogenous hormones affected follicle-stimulating hormone (FSH) concentrations, but the combination of one or both steroids with bFF reduced FSH secretion. Testosterone and estradiol reduced luteinizing hormone (LH) pulse frequency (there was no synergism), and bFF had no effect. Plasma prolactin concentrations were not affected by any treatment. To locate the central sites of steroid action, castrated rams were bilaterally implanted in the preoptic area (POA), ventromedial nucleus (VMH), or arcuate nucleus (ARC). These implants did not affect FSH or prolactin concentrations, or LH pulse amplitude. The frequency of the LH pulses was not affected by testosterone in any site. Estradiol located in the ARC, but not the POA or VMH, decreased LH pulse frequency. In summary, FSH secretion is controlled by synergistic interactions between inhibin and estradiol or testosterone, whereas GnRH/LH pulse frequency is controlled by testicular steroids. Estradiol acts partly, at least, in the ARC, but the central site of action, testosterone remains unknown.

Animals↗
PubMed1993

Hormone production by the postmenopausal ovary in cases of benign ovarian neoplasia.

OBJECTIVE: The objective of this study was to determine whether hormone production by postmenopausal ovaries containing benign ovarian tumors differed from that of normal postmenopausal ovaries. STUDY DESIGN: The sera of 32 postmenopausal patients were assayed before and after bilateral oophorectomy for estrone, 17 beta-estradiol, androstenedione, testosterone, and dehydroepiandrosterone sulfate. The data from all patients as a group were analyzed, followed by analysis of the data from 15 patients with normal ovaries separately from the remaining 17 patients who had nonfunctioning, benign ovarian tumors. RESULTS: For patients with benign ovarian tumors there was a statistically significant drop in estrone (from a presurgical level of 55.8 +/- 46.3 pg/ml to a postoperative level of 29.9 +/- 10.2 pg/ml, p < 0.03) and 17 beta-estradiol (from 18.6 +/- 14.1 pg/ml preoperatively to 9.8 +/- 3.8 pg/ml postoperatively, p < 0.02). For postmenopausal woman with normal ovaries there was no significant drop in estrone or 17 beta-estradiol after bilateral oophorectomy. There was a statistically significant drop in testosterone and androstenedione after bilateral oophorectomy both for women with normal ovaries and for those with benign tumors. No significant differences in dehydroepiandrosterone sulfate were noted in either group. CONCLUSIONS: These data suggest that, although normal postmenopausal ovaries have not been demonstrated to secrete clinically significant amounts of estrogen, those that contain benign ovarian tumors do secrete small but significant amounts of estrone and 17 beta-estradiol. Both tumor-containing and normal ovaries secrete the androgens androstenedione and testosterone, this secretion not being significantly influenced by the presence of a tumor.

Female↗
PubMed1992

Environmental and social determinants of sexual function in the male lesser mouse lemur (Microcebus murinus).

Environmental factors that regulate the sexual activity of male lesser mouse lemurs have been studied experimentally with more than 60 captive animals over an 8-year period. In this nocturnal Malagasy prosimian, variation in day length is the primary factor controlling seasonal sexual activity. Plasma testosterone concentrations were low (= 9 ng/ml) during short days and reached 60 ng/ml during long days (> 12-hour day). This cyclic pattern persists unchanged when artificial photoperiodic rhythms are applied and is not altered by ageing. The timing of puberty is also regulated by photoperiodic changes. Nevertheless, the sexual activity of the male lesser mouse lemur can be dramatically modified by the social environment. In heterosexual groups, behavioural and physiological components of sexual activity are depressed in all males except the dominant one, whose aggressive interactions are always successful. Intermale sexual inhibition was shown to be mediated by chemical cues present in the urine of dominant or isolated males but not in urine of subordinate individuals. The inhibitory signals possess lipophilic properties and are not contingent on the gonadal activity of the urine donor but are linked to adrenocortical activity. By contrast, chemical signals stimulating the reproductive function of all males are found in the urine of females, the presence of which is required for the establishment of clear dominance among grouped males. Endocrine mechanisms underlying intermale sexual inhibition by chemical cues were analysed. Variations in prolactin strongly suggest that olfaction interacts with the photoperiodic regulation of reproductive function, leading to changes in the sensitivity of the negative feedback effect of testosterone on gonadotrophin secretion. Inhibitory or stimulatory effects of chemical signals are discussed in the context of their functional significance for wild populations.

Aggression↗
PubMedDate not supplied

Developmental changes in testosterone production by the rat testis in vitro during late fetal life.

The age-related evolution of the in vitro capacity of the rat testis to produce testosterone and to respond to luteinizing hormone (LH) during 3 and 24 h incubation was studied from day 18.5 to day 21.5 of fetal life. Basal testosterone production by testes from 18.5-day-old fetuses was significantly higher than production by testes from 20.5- and 21.5-day-old fetuses when secretion was expressed as either per testis or per microgram of testicular protein. When maximal LH-stimulated testosterone secretion was expressed on a per testis basis, it was significantly lower for day 18.5 testes than for day 20.5 and 21.5 testes. However, when it was expressed on the basis of testicular protein content, it decreased significantly between days 18.5 and 20.5. Basal and LH-stimulated secretions displayed the same time-related decrease throughout 24 h of incubation for the three ages studied. The dose-response curves for LH showed that the sensitivity was similar for day 18.5 and 20.5 testes (ED50 = 10 vs. 14 ng/mL, respectively). These results showed an age-related decrease in testicular steroidogenic capacity without a change in the coupling efficiency of LH receptor to testosterone production during late fetal life in rats.

Animals↗
PubMed2005

Testosterone rapidly stimulates insulin release from isolated pancreatic islets through a non-genomic dependent mechanism.

The action of testosterone on the 45Ca2+ uptake and insulin secretion was studied in short-term experiments using isolated pancreatic islets of Langerhans. Testosterone (1 microM) stimulated 45Ca2+ uptake within 60 seconds of incubation on similar proportion than tolbutamide. Also, the hormone rapidly increased insulin release (34%; 180 seconds) on the presence of non-stimulatory concentrations of glucose (3 mM). Impermeant testosterone-BSA significantly stimulated the secretion of insulin to a lower percentage (10%). The action of the hormone is specific--neither 17beta-E2 nor progesterone stimulated insulin secretion in the presence of 3 mM glucose. The action of testosterone on insulin secretion was dose-dependent, and at rat plasma physiological concentrations (25 nM), stimulus was 17% (p < 0.05). In conclusion, in isolated pancreatic islets experiments, physiological concentration of testosterone rapidly stimulate insulin secretion and 45Ca2+ uptake through a membrane bound mechanism.

Animals↗