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PubMed1975

Persistent testicular delta5-isomerase-3beta-hydroxysteroid dehydrogenase (delta5-3beta-HSD) deficiency in the delta5-3beta-HSD form of congenital adrenal hyperplasia.

A partial testicular defect in testosterone secretion has been documented in a pubertal male with a congenital adrenal hyperplasia due to hereditary deficiency of the delta5-isomerase-3beta-hydroxysteroid dehydrogenase enzyme complex (delta5-3beta-HSD). Diagnosis of the enzymatic defect is based on the clinical picture of ambiguous genitalia and salt-losing crisis in infancy, together with high urinary delta5-pregnenetriol and plasma dehydroepiandrosterone when the patient was taken off replacement corticoid treatment. No hormonal response to ACTH or salt deprivation was demonstrable. In addition, in vivo studies revealed a partial enzymatic defect in the testis. Although plasma testosterone was low-normal (250 ng/100 ml), plasma delta5-androstenediol was markedly elevated and rose to a greater extent than testosterone after human chorionic gonadotropin administration. In vitro testicular incubation studies suggested a testicular delta5-3beta-HSD enzyme defect with less delta4 products formed from delta5 precursors than in a control testis. Histochemical studies of the testis were also consistent with this defect. Testicular biopsy revealed spermatogenic arrest, generally diminished Leydig cells, but with focal areas of Leydig cell hyperplasia as well as benign Leydig cell hyperplasia as well as benign Leudig cell nodules within the spermatic cord. In vivo studies of steroid metabolism suggested intact peripheral or hepatic delta5-3beta-HSD activity. These studies imply that delta5-3beta-HSD activity differs in the gonad, adrenal, and peripheral organs. These findings are compatible with the concept that the enzyme complex consists of subunits and/or that enzymes in these organs are under different genetic control.

17-alpha-Hydroxypregnenolone↗
PubMed2000

A possible role for reproductive hormones in newborn boys: progressive hypogonadism without the postnatal testosterone peak.

Healthy boys have a considerable production of reproductive hormones during the first postnatal months, the biological significance of which is poorly understood. We report on cases of male infants with hypogonadism (hypogonadotropic hypogonadism, n = 1; panhypopituitarism, n = 2) who showed lack of penile growth and involution of the scrotum. In two boys, diagnoses were obtained in early infancy and hormonal measurements at 3-4 months of age showed serum testosterone levels below detection limits in both low inhibin B (37 and 199 pg/mL, respectively; normal range, 193-563 pg/mL) and low to undetectable gonadotropins [LH, undetectable and 0.07 IU/L (normal range, 0.65-2.69 IU/L), respectively; FSH, 0.18 IU/L in both (range, 0.86-2.52 IU/L)]. In a third boy, gonadotropin deficiency was diagnosed at 3 yr of age by undetectable serum levels of FSH and LH both before and after stimulation with GnRH. All cases required hormonal treatment with testosterone, administered as suppositories in daily doses between 1 and 5 mg, which reintroduced male genital development. Our observations suggest that normal phallic and scrotal development in humans is dependent on intact testosterone secretion during early infancy. Additionally, the diagnosis of gonadotropin deficiency may be established in a short-time window postnatally by measurement of spontaneous serum concentrations of reproductive hormones.

Adaptor Proteins, Signal Transducing↗
PubMed1989

Morphological and functional responses of rat Leydig cells to a prolonged treatment with human chorionic gonadotropins.

The morphological and functional responses of rat Leydig cells to a 3- and 6-day treatment with human chorionic gonadotropins (hCG) (10 IU/kg/day) were investigated by morphometric and radioimmunological techniques. hCG-administration induced a notable time-dependent enhancement in the steroidogenic capacity and growth of Leydig cells; this last was almost exclusively due to hypertrophy (and not to hyperplasia). The volume of mitochondrial and peroxisome compartments, as well as the surface area per cell of mitochondrial cristae and smooth endoplasmic reticulum (SER) were significantly increased after hCG treatment, and showed a highly significant positive linear correlation with both basal and stimulated testosterone production by isolated Leydig cells of the contralateral testis. Also the volume of nuclei and lipid-droplet compartment and the surface area per cell of Golgi apparatus displayed a notable hCG-induced rise, but they did not correlate with testosterone secretion. These findings suggest that, in addition to mitochondria and SER, in which the enzymes of steroid synthesis are located, peroxisomes are also specifically involved in the secretory activity of rat Leydig cells.

Animals↗
PubMed2001

Leptin: a possible metabolic signal affecting reproduction.

Since its discovery in 1994, leptin, a protein hormone synthesized and secreted by adipose tissue, has been shown to regulate feed intake in several species including sheep and pigs. Although a nimiety of information exists regarding the physiological role of leptin in rodents and humans, the regulation and action of leptin in domestic animals is less certain. Emerging evidence in several species indicates that leptin may also affect the hypothalamo-pituitary-gonadal axis. Leptin receptor mRNA is present in the anterior pituitary and hypothalamus of several species, including sheep. In rats, effects of leptin on GnRH, LH and FSH secretion have been inconsistent, with leptin exhibiting both stimulatory and inhibitory action in vivo and in vitro. Evidence to support direct action of leptin at the level of the gonad indicates that the leptin receptor and its mRNA are present in ovarian tissue of several species, including cattle. These leptin receptors are functional, since leptin inhibits insulin-induced steroidogenesis of both granulosa and thecal cells of cattle in vitro. Leptin receptor mRNA is also found in the testes of rodents. As with the ovary, these receptors are functional, at least in rats, since leptin inhibits hCG-induced testosterone secretion by Leydig cells in vitro. During pregnancy, placental production of leptin may be a major contributor to the increase in maternal leptin in primates but not rodents. However, in both primates and rodents, leptin receptors exist in placental tissues and may regulate metabolism of the fetal-placental unit. As specific leptin immunoassays are developed for domestic animals, in vivo associations may then be made among leptin, body energy stores, dietary energy intake and reproductive function. This may lead to a more definitive role of leptin in domestic animal reproduction.

Animals↗
PubMed2004

Gender and the use of neuroleptics in schizophrenia.

INTRODUCTION: The oestrogen hypothesis proposes that the lower need for neuroleptic drugs in female schizophrenia patients is caused by the antidopaminergic effect of oestrogens, and that when oestrogen production decreases at menopause, the need for neuroleptic drugs increases in female schizophrenia patients. SUBJECTS AND METHOD: The oestrogen hypothesis was tested in a sample of 4338 schizophrenia patients (DSM III R), who were discharged from hospital and followed up for 3 years. Prescribed daily doses of neuroleptics (DDN) were recorded and converted to chlorpromazine equivalents. RESULTS: Males had higher DDN than females. When the age at first admission (AFA) was controlled, DDNs were higher in males than in females in all age groups. In addition to AFA, DDNs were associated with duration of illness (DUI), education, smoking and clinical status as well as with concurrently prescribed antidepressants, anti-manics, sedatives and hypnotics, but these factors did not explain the gender differences in DDN. CONCLUSIONS: The results did not support the original oestrogen hypothesis. It is proposed that testosterone secretion may explain why male schizophrenia patients are prescribed higher DDNs than female patients. Ageing processes in the central nervous system (CNS) may explain why DDNs decrease after middle age in both genders.

Adolescent↗
PubMed2001

Testosterone levels in healthy men and the relation to behavioural and physical characteristics: facts and constructs.

This review summarises the correlations between testosterone levels and male physical appearance and behaviour. Methodological shortcomings concerning the measurement of testosterone could limit the value of these findings. In addition, testosterone measured in body fluids represents only one step in the cascade of action from production to biological effect, and could therefore provide only a limited view of the complexity of physiological events. Testosterone levels are influenced by conditions that are partly controlled or initiated by the hormone itself, but also by circumstances beyond hormonal or individual control. Different kinds of behaviour are not only subject to influence by environment, but also androgens can reinforce the particular kind of conduct and the behavioural impact can wield negative or positive feedback on testosterone secretion. Therefore, both generalisation and individualisation of study results will lead to doubtful conclusions and prejudices. Results of such studies must be viewed with caution, and over-simplification as well as over-interpretation should be avoided.

Aggression↗
PubMed1987

Effect of local heating of the rat testis on the levels in interstitial fluid of a putative paracrine regulator of the Leydig cells and its relationship to changes in Sertoli cell secretory function.

Rat testes were exposed to heat (43 degrees C) for 15 or 30 min to induce moderate or severe disruption of spermatogenesis, respectively. Over 3-42 days after treatment, testicular morphology and weight, the serum concentrations of FSH and the concentrations in interstitial fluid of testosterone, androgen-binding protein (ABP) and a factor(s) capable of stimulating Leydig cell testosterone secretion were monitored. Moderate seminiferous tubule damage induced by 15 min heat exposure caused a small decrease (20%) in testicular weight, but did not affect the other measures, other than transiently. In contrast, after exposure of testes to heat for 30 min there was a major and progressive decline in testicular weight throughout the experimental period, reaching 39% of control values by 42 days. In these animals, the serum concentrations of FSH were significantly increased (P less than 0.01) throughout the period of study as also where the serum and interstitial fluid concentrations ABP (P less than 0.05-0.01) and levels of interstitial fluid factor (P less than 0.01). It is concluded that the activity of the interstitial fluid factor(s) can be increased by inducing severe but selective disruption of spermatogenesis, whereas moderate disruption has no effect. Moreover, as ABP secretion into interstitial fluid was increased after severe but not moderate disruption, this suggests that in such animals proportionately more ABP may be secreted via the base of the Sertoli cell. The parallel changes in activity of the interstitial fluid factor(s) and concentrations of ABP in interstitial fluid also provides further circumstantial evidence that these products may have a common (Sertoli cell) origin.

Androgen-Binding Protein↗
PubMed1996

The rat thymus contains a heparin-binding factor that modulates steroidogenesis in the testis.

Thymus development and function are under the influence of hormones secreted by the gonads and pituitary. On the other hand, thymus is crucial for the development of reproductive capacities in female and male rats and we have shown that a factor derived from the prepubertal rat thymus has antigonadotropic effect in ovarian and testis cells in vitro. In the present paper we show that the rat thymic factor which modulates gonadotropin action in the gonads is an heparin-binding factor. This capacity was also used as a useful tool to obtain this activity from semipure extracts. An acetone extract was prepared from 15 day old male rats and subjected to molecular filtration chromatography. The activity, of those fractions was investigated in a testis cells bioassay, by measuring testosterone secretion under basal and hCG-stimulation. Active fraction were processed in an heparin-Sepharose affinity column. We found that fractions that eluted with 0.6 and 2M NaCl/10mM Tris had biological specific activity. The electrophoretic procedure showed that the apparent molecular weight of the Heparin Sephadex binding factor is 60 kDa. Since this factor was obtained from a protein peak that eluted in the volume of carbonic anhidrase a dimerization process could be involved. Present results show that the rat thymus has an heparin-binding factor that interacts with hCG in testis cells. This factor could play an interesting role in the mutual influence between thymus and gonads.

Animals↗
PubMedDate not supplied

Gonadotroph and Leydig cell responsiveness in the male rat. Effects of experimental left varicocele.

Previous experiments have found that experimental left-sided varicocele (ELV) in rats is associated with significant bilateral reductions in intratesticular testosterone concentrations. The current experiments were performed to determine the source of this endocrinopathy. Sensitivity and responsivity of Leydig cells and gonadotrophs were determined in control male rats and in those with ELV. Initially, dose-response relationships were determined for luteinizing hormone (LH) stimulation of testosterone secretion by Leydig cells and for luteinizing hormone releasing hormone (LHRH) stimulation of LH secretion by gonadotrophs. Maximally (ED100) and half-maximally (ED50) stimulating doses of LH and LHRH were selected from these studies and administered to sham-operated and ELV rats 30 days after the operation to induce ELV. Leydig cell and gonadotroph sensitivity (response to ED50) and responsivity (response to ED100) to LH and LHRH, respectively, were determined. Responsivity of Leydig cells in control and ELV rats was similar. Responsivity of gonadotrophs to LHRH was significantly suppressed in ELV animals, but the physiologic relevance of this singular finding is unclear. It is possible that the previously determined ELV-associated decrease in intratesticular testosterone concentrations is subsequent to a wash-out phenomenon that follows the increased testicular blood flow that also is known to be associated with ELV.

Animals↗
PubMed2000

Absence of correlation between in situ expression of cytochrome P450 17alpha hydroxylase/lyase and 3beta-hydroxysteroid dehydrogenase/(Delta5-4) isomerase messenger ribonucleic acids and steroidogenesis during pubertal development in the rat testis.

Changes in expression of Leydig cell 3beta-hydroxysteroid dehydrogenase (3betaHSD) and 17alpha-hydroxylase/C17-20 lyase (P450(17alpha)) messenger RNA (mRNA) during pubertal development have not been well characterized in the rat. In the present study, expression of 3betaHSD and P450(17alpha) were determined in frozen sections of testes of immature (days 21 and 28), pubertal (days 45 and 60) and adult (day 90) rats by in situ hybridization using digoxigenin-labeled riboprobes and quantified densitometrically. Measures of steroidogenesis in this study, 3betaHSD and P450(17alpha) enzyme activities per testis and plasma testosterone concentration, increased during pubertal development, peaking at 45-60 days of age. Expression of 3betaHSD protein, a marker for Leydig cell function, was abundantly immunolocalized to the interstitial compartment of the testis. Quantified densitometrically, the amount of 3betaHSD protein did not vary significantly during pubertal development. Transcripts of 3betaHSD and P450(17alpha) were expressed abundantly by clusters of immature Leydig cells in immature animals. However, in contrast to measures of steroidogenesis during pubertal development, mRNA of 3betaHSD and P450(17alpha) decreased to undetectable levels at the age of 45 and 60 days, respectively. The decline in mRNA of 3betaHSD and P450(17alpha) was confirmed by Northern analysis. Expression of 3betaHSD and P450(17alpha) transcripts rebounded in the adult at 90 days and were comparable to levels of expression observed in immature animals. These results show that during pubertal development the steady-state accumulation of mRNA of 3betaHSD and P450(17alpha) are not correlated with accumulation of 3betaHSD protein, enzyme activities of 3betaHSD and P450(17alpha), or testosterone secretion. Possible explanations of the depletion of transcripts during pubertal development include: specific inhibition of transcription, increased mRNA instability, or high translational activity.

Androgens↗
PubMedDate not supplied

A study of the effect of B-EP and naloxone on the function of the hypothalamo-pituitary-testicular axis of the rat.

To investigate whether endogenous opioid peptides (EOP) play an important role in intragonadal regulation of testicular function and regulation of the hypothalamic-pituitary-gonadal axis of the male rat, the authors employed two principal methods: culture of testicular Leydig cells and Sertoli cells, and in vitro perifusion of hypothalamo-pituitary Leydig cells of the adult rat. The results demonstrated that incubation of Leydig cells with B-endorphin (B-EP 10(-9) = 10(-6) mol/L) or naloxone (NAL 10(-5) = 10(-8) mol/L) manifested no significant changes of non-stimulated or hCG-stimulated testosterone secretion both in 20 and 60 day-old rats. Similar results were obtained when the cells were treated with B-EP (10(-10) = 10(-7) mol/L) for 48 h during culture. Pretreatment of incubated Leydig cells with B-EP in similar concentrations for 48 h showed no effect on the response to hCG stimulation. In addition, treatment with B-EP in vitro for 24 or 72 h manifested no effects on estradiol production by aromatization of cultured Sertoli cells. Neither NAL 10(-5) given in vitro nor NAL (5 mg/body weight) injected subcutaneously 1 h before decapitation affected LH and testosterone release from the perifused hypothalamo-pituitary Leydig cells system. These results could not support the hypothesis that B-EP is a local regulator of testicular function. The physiological significance of EOP in regulating the function of gonadal axis of adult male rat remains to be investigated further.

Animals↗
PubMed2004

Suppressing reproductive activity in horses using GnRH vaccines, antagonists or agonists.

There are a number of situations in which it is desirable to suppress part or all of the reproductive endocrine system in a horse, notably the competing animal whose tractability during training, or performance during competition, is compromised by the expression of sexual or aggressive behavior. The current therapeutic approaches to reproductive endocrine suppression include gonadectomy and progestagen administration, where the former carries surgical risks and entails irreversible loss of breeding potential, and effective progestagen therapy requires frequent administration for extended periods and is banned in some competing animals as potentially anabolic. In this context, preventing the action of gonadotrophin releasing hormone (GnRH) by blocking its pituitary receptors is an attractive alternative for reversibly rendering mares anestrus or depressing testosterone secretion or spermatogenesis in stallions. This paper reviews the data on effects, efficacy, reversibility, and side effects of GnRH vaccines, antagonists, and agonists for suppressing reproductive activity in horses, within the context of their potential place in the pharmacological armoury of the veterinary clinician.

Anestrus↗
PubMed1999

Female development in mammals is regulated by Wnt-4 signalling.

In the mammalian embryo, both sexes are initially morphologically indistinguishable: specific hormones are required for sex-specific development. Mullerian inhibiting substance and testosterone secreted by the differentiating embryonic testes result in the loss of female (Mullerian) or promotion of male (Wolffian) reproductive duct development, respectively. The signalling molecule Wnt-4 is crucial for female sexual development. At birth, sexual development in males with a mutation in Wnt-4 appears to be normal; however, Wnt-4-mutant females are masculinized-the Mullerian duct is absent while the Wolffian duct continues to develop. Wnt-4 is initially required in both sexes for formation of the Mullerian duct, then Wnt-4 in the developing ovary appears to suppress the development of Leydig cells; consequently, Wnt-4-mutant females ectopically activate testosterone biosynthesis. Wnt-4 may also be required for maintenance of the female germ line. Thus, the establishment of sexual dimorphism is under the control of both local and systemic signals.

Animals↗
PubMed1996

Testicular injection of 5,6-dihydroxytryptamine or vasectomy interferes with the local stimulatory effect of oxytocin on testicular steroidogenesis in immature rats.

Previous studies indicated that in immature rats testicular administration of oxytocin stimulates testicular steroidogenesis. In the present study, testicular treatment with oxytocin (50 ng) was combined with pharmacological or surgical denervation of the testis in hemigonadectomized immature rats. For denervation 5,6-dihydroxytryptamine (160 micrograms/testis), a substance that destroys serotoninergic neuronal elements, was injected intratesticularly or vasectomy was performed, which also includes transection of the inferior testicular nerve. In 9-day-old animals both vasectomy and pretreatment of the testis with 5,6-dihydroxytryptamine prevented the oxytocin-induced rise in serum testosterone concentration. In addition, intratesticular injection of oxytocin combined with vasectomy resulted in a significant increase in in vitro basal testosterone secretion of the testis. A similar effect was not observed in the 5,6-dihydroxytryptamine-pretreated group receiving oxytocin. The results indicate that testicular innervation is involved in the control of local peptide effects, and data further suggest a differential role of these neural elements in intratesticular regulatory processes.

5,6-Dihydroxytryptamine↗
PubMed1988

Pharmacological studies on androgen suppression in therapy of prostate carcinoma.

In hormone-dependent prostate carcinoma, androgens can be suppressed into the castrate range by LHRH agonists. Testosterone secretion is blocked at two levels: testicular androgens and adrenal androgens. In humans, the contribution of testicular androgens is about 95%, whereas in the rat, the adrenal androgen secretion is negligible. Pharmacological studies were performed on the suppressive effect of the LHRH agonist, buserelin on androgen-dependent organs in adult rats. The reduction in pituitary and testicular binding capacity was monitored during treatment by injection, or by long-term infusion. Marked differences in suppressive mechanisms activated by the different regimens were observed. Changes in testicular steroid biosynthesis were analysed by incubation of testes after treatment with HCG, measuring the spectrum of C21/C19-steroids in incubation media. In particular, the levels of intraprostatic androgens were determined during treatment with daily buserelin injections, or with sustained release formulations of buserelin. The tissue content of testosterone and 5-alpha-dihydrotestosterone (DHT) were both markedly lowered. In castrate rats, stimulation of adrenal function by ACTH infusion had no effect on the prostate weight or intratesticular T/DHT content. Combination therapy during the initial phase of treatment by an androgen receptor blocker (cyproterone acetate) and buserelin (infusion or implants) was more effective to suppress prostate weight and intra-prostatic T/DHT content than therapy with the single compounds alone. Spermatogenesis and fertility were suppressed after prolonged treatment periods of 6-12 months; the testicular atrophy was not reversible in these long-term injection studies. Similar studies in dogs and monkeys have shown a different result: inhibition of spermatogenesis was fully reversible. It is concluded that studies on the mechanism of androgen suppression by LHRH agonists and the effects on androgen dependent organs provide useful information for the improvement in therapy of hormone-dependent prostate carcinoma.

Androgen Antagonists↗
PubMed1987

Prolactin and antiprolactin receptor antibody inhibit steroidogenesis by purified rat Leydig cells in culture.

The in vitro effects of ovine PRL (oPRL) on testicular testosterone synthesis were determined using isolated, collagenase-dispersed, adult rat Leydig cells in culture. oPRL (50-1000 ng/ml) had no effect either on basal or on LH (50, 100 or 2000 pg/ml)-stimulated testosterone secretion by Leydig cells in short-term culture (4 h). 125I-oPRL binding studies revealed a single class of high affinity sites (Ka 8.7 nM) with a low capacity (Bmax 6.7 fmol/mg protein identical to approximately 980 sites/Leydig cell). Isolated Leydig cells were further purified on a continuous Percoll gradient and cultured in serum-free medium, at 34 degrees C, in 5% CO2 and 95% air. After 3 days of culture, the media were collected, the cells washed and then stimulated with hCG (3 ng/ml) for 3 h. oPRL (1-1000 ng/ml) added at plating, caused a log dose-dependent inhibition of testosterone accumulation during the 3-day culture period; the highest and most consistent inhibition (31%) was with 500 ng/ml oPRL. hCG increased the sensitivity to the inhibitory effect of PRL, 10 ng/ml oPRL causing 40% inhibition and 100 ng/ml causing a maximal inhibition of 50%. PRL in fact caused a reduction in the maximal effect (efficacy) of hCG on steroidogenesis, without significantly affecting the ED50 (sensitivity). The effects of an antiPRL receptor antibody raised by the antiidiotypic route and previously shown to bind to rat testis PRL receptors were tested. The antiPRL receptor IgG (13 micrograms/ml) mimicked the PRL inhibitory effect and acted synergistically with PRL (100 ng/ml) in inhibiting both testosterone accumulation in 3-day cultured Leydig cells and their subsequent response to hCG. In summary, a clear inhibitory effect of PRL and a synergistic effect of antiPRL receptor antibody were demonstrated on testosterone synthesis by rat Leydig cells in 3-day culture.

Animals↗
PubMed1991

Combination of a GnRH agonist with an antiandrogen or bromocriptine in the treatment of prostatic cancer; slight potentiation of antigonadal effects.

The effect of combined treatment with a GnRH agonist (buserelin depot, BUS, 6.6 mg every 2 months) with an antiandrogen (cyproterone acetate, CPA, 300 mg day-1) or a prolactin-suppressing agent (bromocriptine, BR, 20 mg day-1) on pituitary-testicular function were studied in patients with advanced prostatic carcinoma. The patients (n = 5-6 per group) were treated in this fashion for 6 months and thereafter orchidectomized. Serum testosterone and gonadotrophin responses were followed during treatment, and histology and certain endocrine parameters were studied using testicular tissue obtained at orchidectomy. Serum LH was suppressed in all treatment groups from mean levels of 4-6 IU l-1 to less than 0.1 IU l-1, whilst serum FSH levels decreased in all groups during the first month of therapy from 4.5-7 to 1-2 IU l-1, but recovered thereafter. Only minor increases in serum gonadotrophin levels were evident 3 months after castration. No differences in gonadotrophin responses were seen between the different treatment groups. Serum levels of testosterone were suppressed from 15-20 nmol l-1 to the castrate range (approximately 1 nmol l-1), in each of the treatment groups. Testicular weight decreased significantly more (P less than 0.05) in the BUS + CPA group, compared to the other treatments. No differences were found in the testicular concentration of testosterone, or LH and FSH receptors between the three treatment groups. On histological examination, spermatogenesis was found to be impaired severely in all groups, with the lowest Johnsen score in the BUS + BR group (2.16 +/- 0.13, vs. 2.73 +/- 0.25 with BUS alone, P less than 0.05). Seminiferous tubular diameters were reduced similarly in all treatment groups. In conclusion, the combination of CPA or BR with BUS in the treatment of prostatic carcinoma does not potentiate the suppression of gonadotrophin or testosterone secretion, evidently because the GnRH agonist exerts a maximal suppressing effect. However, other antigonadal effects were enhanced slightly, including suppressed testicular weights by CPA and further suppression of spermatogenesis by BR.

Adult↗