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PubMedDate not supplied

Evidence that estrogen regulation of testosterone secretion in adult rams is mediated by both indirect (gonadotropin dependent) and direct (gonadotropin independent) means.

Involvement of endogenous estrogen in the regulation of gonadotropin and testosterone secretion was investigated in adult rams. Groups of four rams were either passively immunized against estradiol or treated with the antiestrogen tamoxifen for 2 weeks during the breeding season (October). Circulating testosterone levels in immunized rams increased eight-fold to supraphysiologic values as episodic elevations and baseline levels increased in magnitude; only moderate increases in LH peak frequency and magnitude occurred, and prolactin fell to undetectable levels. Tamoxifen treatment was not associated with changes in mean hormone levels, although there was a tendency toward reductions in the magnitude of episodic LH and testosterone secretion. When rams were challenged with exogenous GnRH and LH, a greater testicular endocrine response was observed in the immunized rams and the pituitary endocrine response was delayed in the tamoxifen-treated rams. Results indicate that in the ram 1) circulating levels of estradiol provide negative feedback signals of different intensities to the testis and the hypothalamic-pituitary axis and 2) tamoxifen exerts a mild estrogenic effect when administered at the dose of 25 mg/day.

Animals↗
PubMed1991

The effect of oxytocin on oestradiol-17 beta and testosterone secretion by cultured human granulosa cells.

The effect of oxytocin at different concentrations was tested on the secretion of oestradiol-17 beta and testosterone by cultured human granulosa cells obtained by follicular punctures during in-vitro fertilization (IVF) attempts. Oxytocin had no effect on testosterone secretion, either in the absence or the presence of follicle stimulating hormone (FSH). It had no effect on oestradiol-17 beta in the absence of FSH. However, it decreased the FSH-stimulated secretion of oestradiol-17 beta in a certain number of cases. This inhibitory effect appears to be associated with cells more responsive to FSH and was identified in women found to be successful in achieving pregnancy during IVF attempts.

Androstenedione↗
PubMed1986

Adrenocorticotropin administration increases testosterone secretion in adult male rats.

It appears that the effect of acute administration of pituitary-adrenal hormones on the pituitary-gonadal axis is species-dependent. However, no information is available with regard to the effect of acute adrenocorticotropin (ACTH) administration on testosterone secretion in rats. The present data indicate that acute ACTH administration can increase serum testosterone levels without modifying luteinizing hormone (LH) levels. Since this rise was not observed in castrated rats, it must be assumed that increased serum testosterone was of gonadal origin. The action of ACTH on testosterone secretion was likely an indirect one since there is no evidence at present for a direct, short-term action of the pituitary-adrenal axis on Leydig cell function.

Adrenocorticotropic Hormone↗
PubMed1990

Effects of fungal metabolites on testosterone secretion in vitro.

To study the direct effect of mycotoxins belonging to different chemical classes on testicular function, dispersed interstitial cells from testes of adult gerbils were short-term cultured either in the absence or presence of mycotoxins, and testosterone secretion was measured. When interstitial cells were incubated with T-2 toxin (0.0076-38.3 nM) there was a dose-dependent decrease of testosterone production (r = -0.72, ID50 = 0.042 nM). Since neither progesteronenor DHEA-stimulated testosterone production was affected by T-2 toxin, the observed inhibition of basal secretion was apparently due to a decrease of pregnenolone production and/or conversion of pregnenolone to progesterone. Much higher concentrations of zearalenone or of ochratoxin A were necessary to induce a similar inhibition of steroidogenesis (369 microM and 1838 microM, respectively) when compared to T-2 toxin. In contrast, citrinin or cyclopiazonic acid affected testosterone secretion only slightly, values reaching significant levels at doses of 1.74 nM (citrinin) and 149 nM (cyclopiazonic acid). In the presence of kojic acid (2.63-2633 nM) a significant, though not dose-dependent inhibition of testosterone secretion was observed. From these experiments it is concluded that mycotoxins of distinct chemical structure act directly on testicular tissue, presumably by inhibiting early steps of the steroidogenic pathway.

Animals↗
PubMed1990

Effects of oxytocin and an oxytocin antagonist on testosterone secretion during the oestrous cycle of the goat (Capra hircus).

Oxytocin at a dose of 100 i.u. injected subcutaneously (s.c.) daily to goats between Days 3 and 6 of the oestrous cycle caused a significant increase in testosterone secretion compared with saline-treated animals. An oxytocin antagonist (0.2 micrograms/kg) injected intra-arterially between Days 12 and 18 of the oestrous cycle or simultaneously with oxytocin between Days 3 and 6 blocked the increased release of testosterone and occurrence of oestrus. It is suggested that oxytocin-induced oestrus may occur via testosterone secretion.

Animals↗
PubMed1984

Effects of gonadotrophin-releasing hormone on testosterone secretion by fetal and neonatal rat testes in vitro.

Testosterone production by fetal (20.5 days) and neonatal (1-day-old) rat testes was measured to study the possible direct effect of gonadotrophin-releasing hormone (GnRH) on steroidogenesis in early development. Single gonads were incubated in the presence and absence of GnRH (10(-10) to 10(-6) M) or agonistic analogues (10(-11) to 10(-7) M). For comparison, some testes were incubated with ovine luteinizing hormone (0.001-0.01 microgram oLH1 NIH-LH-S20/ml of medium TC199. No clear evidence of stimulation by an agonist (10(-7) M) was seen with fetal testes, but the lowest concentration (10(-11) M) gave results suggestive of an inhibitory action. Similar experiments with neonatal testes showed stimulation. With the highest concentration of GnRH or agonist the amounts of testosterone produced were about 2-3-fold greater than from control testes. Greater quantities of testosterone were found with testes exposed to LH. Hourly sampling in one experiment showed that significant stimulation of testosterone secretion had occurred within the first hour with GnRH (10(-6) M). It was concluded that fetal-neonatal rat Leydig cells are responsive to GnRH.

Animals↗
PubMed1978

A testosterone-secreting adrenal adenoma.

A third case of a testosterone-secreting adrenal adenoma is presented. It differs from the other 2 cases in additionally having glucocorticoid abnormalities. Clinically, the patient had been considered as having polycystic ovaries and did show some improvement with estrogen therapy. In fact, were it not for enlarging uterine leiomyomata on this therapy which prompted a more in depth investigation to look for alternative therapy, this potentially malignant adrenal lesion may never have been discovered.

17-Hydroxycorticosteroids↗
PubMed1987

Relationship between the exposure of Leydig cells to factor(s) present in testicular interstitial fluid and changes in their capacity to secrete testosterone during culture or after hCG-induced desensitization.

This study has evaluated whether the decrease in capacity of Leydig cells to secrete testosterone that occurs during culture or after desensitization with hCG in vivo, is a consequence of the removal of a stimulatory factor(s) in testicular interstitial fluid (IF) to which Leydig cells are normally exposed. When Percoll-purified rat Leydig cells were cultured for 3 days in vitro, there was a progressive reduction in their ability to respond to hCG in terms of either testosterone or progesterone production. In contrast, culture of the cells in the presence of 10% charcoal-stripped IF maintained responsiveness to hCG either partially or completely. This effect was attributable to a factor(s) in IF with a molecular weight of greater than 30 kDa; a comparable fraction from serum had little or no effect. Crude Leydig cells from rats injected 24 h previously with 50 IU hCG showed a 70% reduction in their testosterone response to hCG in vitro and, compared to controls, increased testosterone production poorly in response to increasing concentrations of IF. However, progesterone secretion was increased considerably in response to IF. As in controls, fractionation of crude Leydig cells from hCG-desensitized rats on Percoll gradients resulted in three bands of Leydig cells, except that the yields of band 2 and 3 cells (containing about 40 and 85% Leydig cells, respectively) were reduced by 75% and 90%, respectively, with the majority of Leydig cells remaining in band 1 (which comprises poorly responsive cells). Band 2 and 3 cells from hCG-desensitized rats were not greatly different to cells from control rats in terms of their testosterone response to hCG +/- IF, although they produced considerably more progesterone. It is concluded that the reduced capacity of Leydig cells to secrete testosterone during culture may be attributable to some extent to the removal of a factor(s) in IF to which the cells are normally exposed. In contrast, the reduced in vivo exposure of Leydig cells to such factors, as occurs after hCG injection, cannot explain the poor testosterone response of these cells when they are isolated and cultured.

Animals↗
PubMed1999

Diurnal rhythm of testosterone secretion before and throughout puberty in healthy girls: correlation with 17beta-estradiol and dehydroepiandrosterone sulfate.

The regulation of androgen synthesis during puberty in females is complicated, with changes in steroidogenic and peripheral interconversion capacity. In the present study we have investigated the diurnal rhythm of testosterone secretion in 56 healthy girls before and during puberty, up to 2 yr postmenarche. The girls' ages ranged between 4.6-16.5 yr, and their height SD scores ranged between -3.6 and +3.7. One to 5 serum profiles (seven samples per 24 h) were taken from each girl for steroid measurements, and a total of 84 serum profiles were obtained. Serum testosterone concentrations were determined using a RIA with a detection limit of 30 pmol/L. The results demonstrate that there is a diurnal rhythm of testosterone secretion during both prepuberty and puberty in girls. The pattern has its nadir in the late evening or just after midnight, with the highest levels in the morning (0600-1000 h). Serum testosterone concentrations in prepubertal girls were significantly lower than those in pubertal girls and were significantly lower in early puberty than in girls in mid- or late puberty. No differences were found in levels between girls in midpuberty or late puberty. Before puberty, serum testosterone concentrations correlated with serum dehydroepiandrosterone sulfate, consistent with the adrenals being the major source of testosterone. After the onset of puberty, a correlation between testosterone and 17beta-estradiol was seen, consistent with the ovaries being the major source of testosterone during puberty. Furthermore, the present study showed that there is a relative hyperandrogenicity in early puberty, with high levels of androgens relative to estrogens.

Adolescent↗
PubMed1990

Intratesticular injection of [D-Met2-Pro5]enkephalinamide suppresses testosterone secretion of the testis of immature rat.

The possible role of enkephalin in the local control of testicular function was studied in neonatal rats. 5- and 10-day old hemicastrated rats were treated intratesticularly with an enkephalin analog [D-Met2-Pro5]enkephalinamide. In 5-day-old rats local injection of different doses (0.1-0.3 micrograms/testis) of the peptide suppressed basal testosterone secretion in vitro in a dose-dependent manner 2 h posttreatment. Intratesticular administration of naloxone prior to enkephalin treatment prevented the decrease in basal testosterone production induced by the opioid agonist. In 10-day-old animals intratesticular injection of 1.0 and 3.0 micrograms/testis of enkephalinamide reduced serum testosterone concentration and basal testosterone secretion in vitro. Systemic injection of the peptide produced no change in steroidogenesis. These results suggest that enkephalins might be among the intratesticular factors regulating Leydig cell functions.

Animals↗
PubMed1986

A model for the control of testosterone secretion.

We produce here a model to explain the control of testosterone secretion. In this model the hypothalamic secretion of the hormone LHRH (luteinizing hormone releasing hormone) is controlled by a combination of local testosterone concentration and of the local concentration of the pituitary hormone LH (luteinizing hormone). Since LHRH stimulates the release of LH, and LH in turn stimulates the release of testosterone, the three hormones constitute a three-component "feedback" network. We show how this model is able to account for the pulsatility of the release of these three hormones. Furthermore, the model is consistent with results obtained from a wide range of experimental manipulations of the system. For example, it accounts for the changes observed in hormone release patterns after castration. In particular, it follows that no "neural clock", or "neural pulse-generator", is required to force the system into pulsatile behaviour.

Gonadotropin-Releasing Hormone↗
PubMed1986

Nonneoplastic gonadal testosterone secretion as a cause of vaginal cell maturation in streak gonad syndrome.

Endocrine studies were carried out on 3 patients with streak gonad syndrome, 2 of whom had slight proliferative vaginal smear patterns, and the 3rd had slight hirsutism with increased muscle mass but an atrophic type vaginal smear pattern. Simultaneous sampling of peripheral, adrenal and streak gonadal venous blood revealed mildly increased testosterone secretion by the streaks in the 2 patients who had proliferative cytohormonal patterns. Histologic examination of their streak gonads showed hilus cell hyperplasia. It might be suggested that hilus cell hyperplasia was the source of the increased testosterone secretion in these 2 patients and thus resulted in slight maturation of the vaginal epithelium.

Adult↗
PubMed1994

Histomorphology, oLH and hCG receptors, and testosterone secretion in vitro in Rambouillet rams from lines in which females had been selected for low or high reproductive rate.

The objective of this study was to determine whether gross or histomorphological components of the testes, capacity and dissociation constants (Kd) of testicular oLH and hCG receptors, and gonadotrophin-stimulated testosterone secretion in vitro differed among Rambouillet rams from lines selected for low or high female reproductive rate and from rams of a random-bred control line. Lines had been selected for approximately 20 years. Data were collected from 22-month-old rams during the late breeding season. Rams among lines did not differ (P > 0.05) in gross testicular characteristics or most histomorphological characteristics. However, the percentage volume of interstitial vascular tissue was greater (P < 0.05) for rams from lines selected for low female reproductive rate than for rams from lines selected for high female reproductive rate. Receptor sites per Leydig cell and binding capacities of oLH and hCG receptors per testis, per gram of parenchyma, and per milligram of membrane protein did not differ (P > 0.05) among lines. The Kd values for oLH and hCG receptors did not differ (P > 0.05) among lines; however, receptor sites per Leydig cell, capacities of testicular parenchyma to bind gonadotrophin and Kd values were higher (P < 0.05) for oLH than for hCG receptors. Total oLH- and hCG-stimulated testosterone secretion in vitro did not differ (P < 0.05) among lines. In conclusion, selection for or against reproductive rate in Rambouillet ewes has not altered gross or most histomorphometric characteristics of the testes of male offspring, with the exception that selection against reproductive rate increased the proportion of testicular volume occupied by vascular tissue within the interstitium.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2001

Developmentally delimited emergence of more orderly luteinizing hormone and testosterone secretion during late prepuberty in boys.

To quantitate changing feedback control in the GnRH-LH/FSH-testosterone axis in male puberty, we here quantitate the orderliness of hormone release patterns using the regularity (pattern-sensitive) statistic, approximate entropy (ApEn), in 46 eugonadal boys representing 6 genitally defined stages of normal puberty. ApEn is a single variable, model-free, and scale-independent barometer of coordinate signaling or integrative regulation within a coupled neuroendocrine axis. Accordingly, we quantitated ApEn of LH profiles obtained by immunofluorometric assay of sera sampled every 20 min for 24 h. LH ApEn declined remarkably between early prepuberty (genital stage I-A: mean bone age, 4.6 +/- 1.6 yr; testis volume, <3 mL for at least 3 succeeding yr) and late prepuberty (genital stage I-C: bone age, 8.7 +/- 1.8 yr; testis volume, <3 mL for up to 1 yr thereafter; P: = 0.00019), which indicates the acquisition of more regular LH release patterns in late prepuberty. Maximal LH orderliness occurred in puberty stage II (bone age, 10.7 +/- 1.0 yr; testis volume, 2.8 +/- 0.4 mL). The LH secretory process was more disorderly in mid- and later puberty (Tanner stages III and IV). Transpubertal variations in testosterone ApEn manifested a similar tempo, i.e. the greatest regularity of testosterone secretion (lowest ApEn) emerged in Tanner genital stage II (P: < 10(-)(7)), with less orderly patterns evident both earlier and later in sexual development. In contrast, FSH ApEn values remained invariant of pubertal status. Analysis of bihormonal coupling using the theoretically related bivariate cross-ApEn statistic disclosed maximal 2-hormone synchrony for LH and testosterone secretion in genital stage II (P: = 0.031), with relative deterioration of coordinate LH and testosterone release patterns both before and after. LH and FSH release became maximally synchronous at the end of prepuberty (genital stage I-C; P: = 0.029), and FSH and testosterone synchrony peaked in pubertal stage III (P: = 0.037). As mean 24-h serum concentrations of LH, FSH, and testosterone rose transpubertally by 35-fold (LH), 68-fold (FSH), and 70-fold (testosterone), respectively, we infer that pubertal developmental stage per se rather than level of hormone output dictates coordinate GnRH-LH/FSH-testosterone secretion. In summary, in eugonadal boys, the regularity of 24-h LH and testosterone secretory patterns undergoes well defined pubertal stage-specific control. No sexually developmentally delimited regulation is inferable for FSH. The concept of temporally biphasic puberty-dependent variations in neurohormone secretory regularity contrasts with the unidirectional rise in daily hormone output. Accordingly, we infer that late prepuberty and early puberty (Tanner genital stages IC and II) embody a physiologically unique sexual developmental window, marked by transiently enhanced LH and testosterone feedback stability in boys. Whether analogous plasticity of hypothalamo-pituitary-gonadal interactions unfolds during female adolescence is not known.

Child↗
PubMed1988

Effects of local heating of the testis on testicular blood flow and testosterone secretion in the rat.

Exposure of one or both testes of rats to heating at 43 degrees C for 30 min resulted in a significant reduction in blood flow per testis, as measured using microspheres. The effects on the testes of unilateral and bilateral heating were similar, although the changes in FSH levels in peripheral blood were in general less marked after unilateral heating. Testicular blood flow fell, along with testicular weight, beginning at 2-4 days and reaching minimum values 14-21 days after heating. Both blood flow per testis and testicular weight were beginning to recover 35 days post-heating and blood flow per testis was normal by 56 days following heat treatment, although testicular weight was still slightly reduced at that time. Heating one or both testes to 42 degrees C produced similar but smaller responses 21 days later, whereas temperatures of 41 degrees C or lower were without effect on the parameters measured, except for some rises in serum LH and FSH. With slight reductions in blood flow, there were corresponding increases in testicular venous testosterone concentration so that testosterone secretion was unaffected. Further reductions in blood flow at 14 and 21 days after heating to 43 degrees C were not fully compensated by an increase in the concentration of testosterone in testicular venous blood, with the result that testosterone secretion fell.

Animals↗
PubMed1987

Existence of calcium channels and intercellular couplings in the testosterone-secreting cells of the mouse.

1. The electrophysiological properties of testosterone-secreting cells (i.e. Leydig cells) in the mouse were studied using patch electrodes. The cells appeared solitarily or in clusters after mechanical dissociation from testes. They were confirmed to be Leydig cells on the basis of 3 beta-hydroxysteroid dehydrogenase staining. 2. Under current-clamp conditions in the whole-cell configuration, Leydig cells immersed in standard saline were able to generate action potential-like responses. The active responses occurred after cessation of membrane hyperpolarization or when cells were held in a hyperpolarized condition and stimulated with depolarizing current pulses. 3. In Leydig cells under voltage clamp, depolarizations more positive than -50 mV evoked transient inward currents which decayed completely during the duration of depolarization (130 ms). No obvious outward currents were evoked by pulses less positive than 30 mV. 4. The inward currents were identified as Ca2+ current, since replacement of external Ca2+ with Mn2+ reversibly diminished the current whereas Ba2+ or Sr2+ substituted for Ca2+. 5. With voltage pulses more positive than 40 mV, outward currents were evoked. The currents were dependent on K+ concentration and were blocked by quinine or tetraethylammonium. The amplitudes of outward currents were increased with raised internal Ca2+ concentration. 6. Single-channel recordings of the outward currents revealed that the unitary conductance was 130 pS when internal K+ was 131-143 mM and external K+ was 5 mM. The open probability of the channel showed marked dependence on the membrane potential and the internal Ca2+ concentration. Thus, the current was identified as being Ca2+- and membrane potential-dependent K+ current. 7. Leydig cells within a cluster possessed distinct intercellular couplings. The mean coupling ratio obtained by applying two patch electrodes to a pair of cells was 0.84. Transfer of injected dye (Lucifer Yellow) to adjacent cells was also confirmed. 8. It was concluded that Leydig cells have at least two kinds of voltage-dependent channels in the membrane. The Ca2+ channel may be activated by physiological changes in membrane potential, leading to an influx of Ca2+. The Ca2+-dependent K+ channel hardly seems to be activated unless the internal Ca2+ concentration increases remarkably. It is presumed that intercellular coupling may play a role in synchronizing or intensifying the endocrine activities of Leydig cells located within a cluster.

Action Potentials↗
PubMed1987

Effect of uni- and bilateral cryptorchidism on testicular inhibin and testosterone secretion in rats.

The effect of uni- and bilateral cryptorchidism on testicular inhibin and testosterone secretion and their relationships to gonadotropins were studied in rats. Mature Wistar male rats weighing approximately 300 g were made either uni- or bilaterally cryptorchid. Testicular inhibin and testosterone content and plasma levels of LH and FSH were examined 2 weeks later. A similar remarkable decrease in testicular inhibin content was found in uni- and bilaterally cryptorchid testes. On the other hand, the testicular testosterone content was significantly decreased only in unilaterally cryptorchid testis with an inverse increase in the contralateral testis. Plasma testosterone levels were normal and plasma LH and FSH increased significantly in both of the cryptorchid groups. These results showed that cryptorchidism impairs both Sertoli and Leydig cell functions. While testosterone production was compensated by increased LH for 2 weeks, neither inhibin secretion nor storage changed in cryptorchid or contralateral testes during the same period.

Animals↗
PubMed2001

Lesion of the insular cortex affects luteinizing hormone and testosterone secretion of rat. Lateralized effect.

The possible involvement of the insular cortex in the neural control of the hypophyseal-testicular axis was studied in male rats. Right- but not left-sided lesion of the insular cortex resulted in a significant decrease in basal testosterone secretion in vitro and serum testosterone concentration. Both right- and left-sided lesions of the insular cortex induced significant increase in serum luteinizing hormone (LH) concentration. Unilateral lesion of the insular cortex on either sides had no effect on serum follicle stimulating hormone (FSH) level. The results indicate that the insular cortex is involved in the control of testosterone and LH secretion. The data further suggest that the right insular cortex plays a predominant role in the control of male endocrine reproductive processes.

Animals↗