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 1,009 records · Page 56Linked to original sources

Antifertility activity of Quassia amara in male rats - in vivo study.

The crude methanol extract of the stem wood of Quassia amara. L. (A-1) significantly caused a reduction in the weight of the testis, epididymis and seminal vesicle, but an increase in that of the anterior pituitary gland. Epididymal sperm counts, serum levels of testosterone, luteinizing hormone (LH) and follicle stimulating hormone (FSH) were significantly reduced when the rats were treated with the extract. Furthermore the basal and LH-stimulated testosterone secretion of Leydig cells isolated from rats pretreated with the extract was inhibited. These changes seemed to be restored eight weeks after the withdrawal from extract treatments. Two compounds - quassin and 2-methoxycanthin-6-one were isolated after fractionation of A-1. Quassin produced similar biological actions as the crude extract while the effects of 2-methoxycanthin-6-one did not seem to differ from those of the control. Quassin appears to be the antifertility principle of Quassia amara.

Animals↗

Oligotriche and quaking gene mutations. Phenotypic effects on mouse spermatogenesis and testicular steroidogenesis.

The phenotypic actions of the oligotriche gene mutation on testicular function have not been elucidated, although it is known that male mice homozygous for the mutation are infertile. In the present study, the effect of the oligotriche gene mutation on mouse testicular function was analyzed by comparing normal and mutant mice. Spermatogenesis was analyzed by enumerating germ cells in seminiferous tubules at specific stages of spermatogenesis and by electron microscopy. Steroidogenic potential was estimated by radioimmunometric determination of testosterone secreted by testes perfused in vitro. Parallel studies were completed for male mice homozygous for the quaking gene mutation, a mutation known to cause male mouse sterility by disrupting sperm tail development. The experimental results suggest that the oligotriche and quaking gene mutations interfere with sperm tail formation by different mechanisms. Testicular steroidogenesis was not affected by either gene mutation. The results provide the first evidence that the oligotriche gene mutation induces male mouse sterility by effecting the complete absence of a sperm tail. This phenotypic action is different from that of the quaking gene mutation.

Animals↗

Ovarian and adrenal steroidogenesis in a virilized patient with gonadotropin-resistant ovaries and hilus cell hyperplasia.

A 26-year-old woman with secondary amenorrhea, temporal balding, and clitoromegaly was found to have both the gonadotropin-resistant ovary syndrome and hilus cell hyperplasia. Simultaneous sampling of peripheral and ovarian venous blood revealed excess ovarian testosterone secretion to be the probable cause of the patient's virilism. The marked response of the ovary to stimulation by luteinizing hormone (LH) coupled with the lack of ovarian follicular development suggested that an isolated resistance of the ovarian follicle to follicle-stimulating hormone (FSH) was present in this patient. The administration of a daily pharmacologic dose of dexamethasone for 14 days was followed by the patient's first menstrual period in 13 years, raising the possibility that autoimmunity may have been involved in this patient's ovarian resistance to FSH stimulation.

Adult↗

Acute effects of anticonvulsant drugs on gonadotropin-stimulated and precursor-supported androgen production in the rat testis.

The possibility of direct inhibition of testicular endocrine function by carbamazepine, phenytoin, or valproate was tested using the rat Leydig cell model in vitro in order to find whether such an effect could contribute to the reduction of plasma free testosterone levels reported in male patients who take antiepileptic medications. With maximally stimulating concentrations of human choriogonadotropin (hCG) or cyclic AMP, testosterone formation was inhibited by 50% in the presence of 40 microM carbamazepine, 350 microM phenytoin, or greater than 1 mM valproate. With submaximally stimulating concentrations of hCG, leading to physiological testosterone secretion rates, half-maximal inhibition occurred in the presence of 15 microM carbamazepine, 180 microM phenytoin, or 900 microM valproate. Only the values for carbamazepine were in the clinically therapeutic range. Further investigation revealed that carbamazepine acted primarily at a target between cyclic AMP formation and cholesterol conversion to androgens. In contrast, phenytoin acted by competitive interaction at the cytochrome P450XVII which converts progesterone to androgens. Valproate had by far the lowest potential to generate adverse effects in this endocrine system.

Androgens↗

A gonadotrophin dependent stromal luteoma: a rare cause of post-menopausal virilization.

A stromal luteoma is an uncommon ovarian tumour in post-menopausal women, which presents rarely with hyperandrogenism and virilization. We present the case of a 64-year-old woman referred for evaluation of virilization which had developed over 5 years. Testosterone, FSH and LH were markedly inhibited following the administration of a GnRH analogue, suggesting a gonadotrophin dependent, testosterone secreting ovarian tumour, which could not be localized with imaging techniques. Surgery revealed normal sized ovaries with no apparent lesions, but microscopic examination showed a small stromal luteoma in the right ovary and severe stromal hyperthecosis in the adjacent and contralateral ovarian stroma. We conclude that stromal luteoma is an uncommon cause of virilization in post-menopausal women. This case illustrates, to our knowledge for the first time, that a stromal luteoma is not autonomous but is gonadotrophin dependent.

Depression, Chemical↗

Endocrinological studies in patients with metastatic malignant testicular germ cell tumours.

In this study, various serum hormone levels were determined in patients with metastatic testicular germ cell tumours. Raised LH levels, due to a cross reaction with hCG in the radioimmunoassay, were observed in 20 out of 29 patients with active disease and were mainly caused by gonadotrophin production in the tumour tissue. Increased LH levels were frequently observed in the patients with non-seminomatous tumours, but were also found in 4 (out of 6) patients with metastatic seminoma. One should, however, preferably use a specific hCG radioimmunoassay in order to measure tumour hCG as a tumour marker with a high diagnostic accuracy. In patients with active disease despite ongoing combination chemotherapy which included LH suppressing medication, serum testosterone remained above 6 nmol/l in 11 out of 16 patients. These patients remained sexually potent, while testosterone values below 6 nmol/l usually were combined with sexual impotence in patients during combination chemotherapy. These data strongly suggest that the tumour hCG has a biological activity, stimulating the remaining testis to increased testosterone secretion in these patients. The serum E2-17 beta levels were slightly to moderately increased in half of the patients with metastatic disease. Markedly increased serum E2-17 beta levels (> 0.30 nmol/l) and very high prolactin values (> 32 micrograms/l) were observed only in patients with high LH levels (> 9.5 micrograms/l) and a large tumour burden. These observations indicate that E2-17 beta and prolactin determinations are of minor value for early detection of tumour manifestations. Serum FSH cannot serve as a tumour marker in patients with testicular germ cell tumours.

Adult↗

Stimulation of sexual behavior in the male rat by galanin-like peptide.

Galanin-like peptide (GALP) is a recently described neuropeptide, which shares a partial sequence identity with galanin but is derived from a separate gene. Central injections of GALP stimulate the secretion of gonadotropin-releasing hormone (GnRH) and luteinizing hormone (LH) and induce the expression of Fos in several brain areas known to regulate male sexual behavior in the rat. We postulated that GALP may also stimulate sexual behavior in concert with its stimulatory effect on the hypothalamic-pituitary-gonadal (HPG) axis. To test this hypothesis, we administered GALP, galanin, or the vehicle (artificial cerebrospinal fluid, aCSF) alone to sexually experienced male rats and assessed the effects of these agents on sexual behavior. We observed that compared to aCSF alone, GALP significantly increased all aspects of male-typical sexual behavior, whereas galanin inhibited all of these same behaviors. To examine whether the stimulatory effects of GALP on sexual behavior were mediated by GALP's stimulatory effects on the HPG axis, we castrated the same male rats and repeated the behavioral experiment. We found that GALP maintained its inductive action on male-typical sexual behaviors in the castrated animals, suggesting that the effects of GALP on sexual behavior are not the result of GALP's ability to stimulate testosterone secretion. These observations suggest that GALP neurons are part of the hypothalamic circuitry controlling sexual behavior in the male rat.

Animals↗

Hormonal pattern and testicular histology in patients with prostatic cancer after long-term treatment with a gonadotropin-releasing hormone agonist analogue.

Seven patients suffering from prostatic cancer were treated with a depot form of D-Trp-6-luteinizing hormone-releasing hormone (LH-RH), a LH-RH agonist analogue (3 mg i.m. every 28 days) for a period of 24-32 months. The peptide induced a sharp and long-lasting inhibition of both gonadotropin and testosterone secretion. A sustained suppression of pituitary and testicular function was observed 40 days after the treatment was suspended. Testicular biopsies performed in all patients showed a marked impairment of Leydig cell mass and a complete spermatogenic arrest with a tubular derangement and fibrosis. Results indicate that the long-term continued gonadotropin-releasing hormone agonist analogue therapy induces not only a functional inhibition of testicular androgenesis but also anatomical testicular damage whose reversibility does not seem to be probable.

Aged↗

Effect of ingestion and inhalation of lead on the reproductive system and fertility of adult male rats and their progeny.

Ninety-day-old Sprague-Dawley rats were intoxicated for 70 d with lead, given either as 0.3% lead acetate in drinking water or by inhalation as 5 mg m-3 lead oxide. Direct or transmitted lead toxicity for the male reproductive system was assessed in the rats and their offspring from pituitary and genital organ weights after exposure, the numbers of Sertoli and germ cells, the number, motility and morphology of epididymal spermatozoa, the levels of plasma testosterone, LH and FSH and fertility tests. Whole blood lead levels were similar after lead ingestion and after inhalation (58.0 +/- 1.7 micrograms dl-1 vs. 51.1 +/- 1.8 micrograms dl-1). Lead acetate ingestion did not affect the reproductive system or fertility of rats. Inhalation of lead oxide did not affect fertility either, but seminal vesicle weight dropped significantly, which might suggest an alteration in the pattern of testosterone secretion. In the male progeny of sires that inhaled lead, the number of epididymal spermatozoa decreased but this did not interfere with fertility. Our results show that for the doses studied, lead inhalation and lead ingestion do not produce strikingly different effects on the male rat's reproductive system. Differences between the present findings and those of others might be due to difference of rat strain or of age at exposure.

Administration, Inhalation↗

Efficacy of perfluorodecalin as an oxygen carrier for mouse and rat testes perfused in vitro.

Perfluorodecalin is a superior artificial oxygen carrier because of its high oxygen dissolving capacity, low toxicity, and short retention times within tissues. However, the instability of perfluorodecalin emulsions has hindered its application in blood substitutes. The present study addressed two questions. First, is perfluorodecalin deleterious to the endocrine function of testes? This question was examined by comparing testosterone secretion by testes perfused in vitro with medium incorporating either perfluorodecalin or erythrocytes as oxygen carriers. Second, can stable emulsions of perfluorodecalin be attained with the new surfactant Butronic U-1? This question was approached by determining the stability of perfluorodecalin emulsions containing either Butronic U-1 or Pluronic F-68, a proven ineffective surfactant. The experimental results support the efficacy of perfluorodecalin emulsions as oxygen carriers for mouse and rat testes perfused in vitro. Perfluorodecalin emulsions formed with Butronic U-1 were stable during the 4-hr perfusions but not during long-term storage.

Animals↗

Novel expression of resistin in rat testis: functional role and regulation by nutritional status and hormonal factors.

Resistin, a recently cloned adipose-secreted factor, is primarily involved in the modulation of insulin sensitivity and adipocyte differentiation. However, additional metabolic or endocrine functions of this molecule remain largely unexplored. In this study, a series of experiments were undertaken to explore the potential expression, regulation and functional role of this novel adipocytokine in rat testis. Resistin gene expression was demonstrated in rat testis throughout postnatal development, with maximum mRNA levels in adult specimens. At this age, resistin peptide was immunodetected in interstitial Leydig cells and Sertoli cells within seminiferous tubules. Testicular expression of resistin was under hormonal regulation of pituitary gonadotropins and showed stage-specificity, with peak expression values at stages II-VI of the seminiferous epithelial cycle. In addition, testicular resistin mRNA was down-regulated by the selective agonist of PPARgamma, rosiglitazone, in vivo and in vitro. Similarly, fasting and central administration of the adipocyte-derived factor, leptin, evoked a significant reduction in testicular resistin mRNA levels, whereas they remained unaltered in a model of diet-induced obesity. From a functional standpoint, resistin, in a dose-dependent manner, significantly increased both basal and choriogonadotropin-stimulated testosterone secretion in vitro. Overall, our present results provide the first evidence for the expression, regulation and functional role of resistin in rat testis. These data underscore a reproductive facet of this recently cloned molecule, which may operate as a novel endocrine integrator linking energy homeostasis and reproduction.

Adipocytes↗

Calcium homeostasis and mineralization in puberty.

Calcium homoeostasis and bone mineralization have been the subject of many studies, but few have dealt with these aspects specifically in puberty. The main observations in our own studies - together with those in other recent reports - are summarized below. According to the aims of the present survey (Chapter 1) the results are grouped as follows: BLOOD MINERAL HOMOEOSTASIS AND ALKALINE PHOSPHATASE. The serum concentrations of calcium, total or ionized, remain remarkably constant throughout puberty, which probably reflects the important functions of the calcium ion. Serum phosphate, however, remain high in childhood, increase slightly with acceleration of growth and pubertal development and the levels then decrease toward adult values. Consequently, the pattern of the product of serum calcium and phosphate, essential for mineralization, follows that of phosphate. Serum magnesium does not change during puberty. The serum concentrations of alkaline phosphatase increase with acceleration in linear growth and pubertal development which has to be taken into consideration, in evaluation of changes in serum AP. Changes in osteoblastic activity, as expressed by AP (and BGP), are closely associated with changes in testosterone secretion with almost simultaneous increases in serum levels of both variables. It is further concluded that longitudinal study designs may add to the understanding of the growth process and rate of changes, whereas cross-sectional data are relevant to establish proper reference ranges. BONE MINERAL CONTENT. The use of photon absorptiometry in determining BMC is a precise, easy, atraumatic and reproducible method. It is shown that forearm BMC has a highly significant correlation to total body bone mineral also in the pubertal period of rapid growth. It should be noted that single measurements of BMC are of little diagnostic value in the presence of wide biological variation. A spurt in mineralization corresponding to that of height in puberty has been known since the development of the BMC technique. It is evident from our data that BMC and indices of body size are only significantly related after the start of the growth spurt. Significant increases of 25% in the BMC have been found in the year prior to PHV progressing with each PH stage. The mean time of maximal increase in forearm BMC occurred some 5 months later than that of testosterone and AP, and changes in these three variables are closely interrelated. The change in the serum concentrations of the two major adrenal androgens did not appear to be related to BMC.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗

Hormones and hormonal target cells in the testis.

Studies over the last few years have greatly increased our knowledge about target cells for sex hormones and gonadotropins in the testis. A diagram illustrating our present state of knowledge is given in Fig. 1. LH is the principle stimulus of testosterone secretion by the Leydig cells. Direct effects of estrogens and androgens on these cells might modulate the response to LH. Androgens are apparently influencing the differentiation and the contractility of peritubular cells. FSH is the principle stimulus for Sertoli cell secretory function before puberty, although androgens are acting synergistically with FSH. After puberty, androgens alone are capable of maintaining on optimal secretory function of the Sertoli cells. In addition to normal secretory activity of the Sertoli cells, direct stimulation of the germ cells by androgens is needed in order maintain spermatogenesis.

Age Factors↗

Use of hypothalamic releasing factors to examine the effects of increased testosterone on pituitary response in a postmenopausal woman. A case report.

Hyperandrogenic states in women may alter hypothalamic pituitary response. The pituitary function of a 64-year-old postmenopausal woman with a testosterone-secreting (T-secreting) ovarian neoplasm was assessed with a combined infusion of ovine corticotropin releasing hormone, 1 microgram/kg; GnRH, 100 micrograms; human growth hormone releasing hormone, 1 microgram/kg; and TRH, 200 micrograms preoperatively when T and estradiol (E2) were elevated, six weeks postoperatively when T and E2 were low and 16 months postoperatively while the patient was on micronized E2 (low T, high E2). The principal findings were a reduction in luteinizing hormone response by both T and E2, no effect of either T or E2 on follicle stimulating hormone and greater growth hormone and TSH responses in an estrogenic milieu.

Estradiol↗

Luteolytic effect of azastene in the nonhuman primate.

The ability to block steroidogenesis with 4,4,17-alpha-trimethylandrost-5-eno[2,3,-d]isoxazol-17-ol (azastene) was studied in 3 different models. Oral administration of 500 mg to rhesus monkeys on different days of their luteal phase induced marked depression of circulating progesterone concentrations, and in some cases early onset of menses. Simultaneous administration of human chorionic gonadotropin (hCG) during the midluteal phase did not overcome the luteolytic effect of azastene. Concentrations of 50 micrograms/ml of azastene inhibited testosterone secretion by decapsulated mice testes in vitro in response to hCG [controls, 1165 +/- 196 ng/ml, azastene, 306 +/- 40 ng/ml (P less than .01)]. Production of progesterone by dispersed luteal cells from rhesus monkey corpora lutea was markedly inhibited by the presence of 25 and 50 micrograms/ml azastene in the incubation media (P less than .05 and less than .01, respectively). The availability of a compound that blocks in vivo and in vitro gonadal steroidogenesis opens a new approach to postcoital contraception in primates because of its luteolytic and interceptive activity. The possible mechanisms of action of azastene are discussed.

Abortifacient Agents↗

Castration increases pulsatile luteinizing hormone release, but fails to diminish mounting behavior in sexually experienced bulls.

We tested the hypothesis that mounting and chemoinvestigatory behaviors are testosterone-dependent in bulls. Eighteen bulls were divided into three treatment groups: intact (I), castrated (C) and castrated+testosterone (T). Sexual behaviors of all bulls were tested with an unrestrained receptive female 1 week prior to and weekly for 4 weeks after castration. Mounts with intromissions, aborted mounts and flehmen responses were quantified for each test period. In addition, patterns of LH and testosterone secretion were assessed at these times. Neither mounts with intromissions nor aborted mounts were affected by treatment. In contrast, numbers of flehmen responses were lower in C bulls than in the other groups following castration. Before castration, concentrations of LH were not different among groups and LH pulse frequency was approximately one pulse per hour. Castration resulted in a 2-fold increase in mean concentrations of LH and a 6-fold increase in LH pulse frequency. Neither mean concentration of LH nor LH pulse frequency changed in I or T bulls. The data fail to support the hypothesis that mounting behavior is T-dependent, but supports the hypothesis that this steroid hormone regulates flehmen behavior in sexually experienced bulls.

Animals↗

Effect of simultaneous local injection of 6-hydroxydopamine and naloxone on the testis of neonatal rats.

The effect of simultaneous intratesticular injection of the opiate receptor antagonist naloxone and the neurotoxic drug 6-hydroxydopamine (6-OHDA) on testicular growth, compensatory testicular hypertrophy, serum testosterone level and basal testosterone secretion in vitro was studied in neonatal rats. In animals with two testes unilateral intratesticular administration of naloxone alone enhanced, while 6-OHDA alone decreased the weight of the treated gonad. In animals treated simultaneously with these two agents the decrease in testicular weight induced by 6-OHDA was partially prevented by naloxone. In hemicastrated animals intratesticular treatment with naloxone enhanced the extent of compensatory testicular hypertrophy. Treatment of the remaining testis with 6-OHDA + naloxone did not interfere with the diminished compensatory testicular hypertrophy observed following 6-OHDA treatment. Data indicate that naloxone can counteract the degenerative effect of 6-OHDA in animals with two testes but not in hemicastrates.

Animals↗

Cultured Sertoli cell-mediated FSH stimulatory effect on Leydig cell steroidogenesis.

To determine the precise role of Sertoli cells in the stimulating effects of follicle stimulating hormone (FSH) on Leydig cell activity, porcine purified Leydig and Sertoli cells were cultured separately or together in a chemically defined medium in the absence or presence of porcine, FSH 50 ng/ml. Leydig cell activity was evaluated using two parameters: human chorionic gonadotropin (hCG) binding sites; and hCG-stimulated cAMP production and testosterone secretion. First, it was found that FSH increases Leydig cell activity in crude Leydig cell preparations (40-60% of Leydig cells), whereas it exerts no effect on purified Leydig cells (greater than 90% of Leydig cells). Second, FSH stimulates the activity of Leydig cells cocultured with Sertoli cells, whereas it remains without effect on purified Leydig cells cultured alone. This stimulating effect of FSH on Leydig cell activity is dependent on the Sertoli cell number in the coculture. These data 1) show that the stimulating effect of FSH on Leydig cell function is mediated by Sertoli cells and 2) support the concept of local control of Leydig cell function originating from Sertoli cells.

Animals↗