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PubMed1978

Effect of chronic administration of estrogen, androgen, or both on serum levels of gonadotropins in adult men.

Ethinyl estradiol (50 micrograms/day) or fluoxymesterone (10 or 20 mg/day), chosen because each is orally active and because fluoxymesterone is probably not converted to an estrogen, were given alone and in combination to adult men over several weeks. Measurements were made of serum FSH, LH, testosterone, and estradiol. The estrogen given alone suppressed serum FSH while the androgen given alone did not; however, the androgen may have enhanced the suppressive effect of the estrogen on the serum FSH. Neither steroid alone changed the serum LH but both together suppressed it. The estrogen alone decreased the serum testosterone, an effect probably mediated by the concomitant fall in serum FSH and a resulting decrease in sensitivity to the constant level of LH; a direct effect of estrogen on the testis seems less likely. The doses of estrogen and androgen used probably had a biologic effect equal to or somewhat above that of endogenously produced estrogen and androgen and thus reflected the maximum physiological effects of the endogenous steroids. Thus, in the chronic physiological control of FSH and LH in adult men, these data indicate that (1) testosterone alone, as an androgen, has little effect on FSH or LH, (2) estradiol (or total estrogen) has a greater suppressive effect on FSH than on LH and by its effect on FSH may indirectly regulate the secretion of testosterone, and (3) testosterone and estradiol together may be involved in the regulation of both FSH and LH.

Adult↗
PubMed1992

Annual changes of testis size, seminiferous tubules and plasma testosterone concentration of wild Sika deer (Cervus nippon yesoensis Heude, 1884) in Hokkaido.

Testis size, seminiferous tubules and plasma testosterone concentrations showed conspicuous annual changes in Sika deer of Hokkaido, Japan. The onset of the spermatogenic process occurred in July or August. Spermatogenic activity had already reached its height in late October, at the beginning of the rutting season, and had begun to decline in late December. Spermatogenesis had stopped in February or March. Plasma testosterone concentrations showed very high levels in late October and early November, but was almost at the basal level in February, March, June and December. The wide individual variation of the plasma levels in October suggest pulsatile secretions of testosterone.

Animals↗
PubMed1989

The uptake of [3H]testosterone and its metabolites by the brain and pituitary gland of the fetal macaque.

Testosterone is secreted by the fetal testis during gestation, and this is thought to influence certain aspects of the brain's subsequent development. To study this action at the neuronal level, nine macaque fetuses were injected with 250 microCi [3H]testosterone via the umbilical vein at about 120 days gestation. After 60 min, samples of brain and peripheral tissue were studied by autoradiography or HPLC. Purified nuclear pellets were prepared, and radioactivity in ether extracts was fractionated by HPLC and identified by coelution with internal standard steroids. Concentrations of radioactivity were significantly higher (P less than 0.05) in the hypothalamus-preoptic area than in amygdala, hippocampus, midbrain, and cerebral and cerebellar cortexes, and most of the radioactivity (75%) in the hypothalamus-preoptic area coeluted with 17 beta-estradiol. Radioactivity coeluting with 17 beta-estradiol was also detected in nuclear fractions from amygdala (44%). In contrast, 80% of the radioactivity extracted from pituitary gland nuclei coeluted with testosterone. Most of the neurons labeled in autoradiograms were located in the hypothalamus and preoptic area, fewer were found in the amygdala, and labeling in the frontal or motor cortex did not exceed chance levels. Results suggested that aromatization and, consequently, estrogen receptors play a role in the effects of testosterone on the hypothalamus and amygdala of the primate fetus at this stage of development.

Amygdala↗
PubMed1981

Effect of LH and FSH on testosterone release from cultured Leydig cells.

The level of testosterone in incubation media of cultures of Leydig cells isolated from mouse testes were measured by specific radioimmunoassay. Luteinizing hormone (LH) in a concentration of 10, 100 and 500 ng per 1 ml of culture medium stimulated the secretion of testosterone very markedly especially after 2 days of culture. LH in the amount of 100 ng ml-1 exerted the most stimulating effect on testosterone production by cultured Leydig cells. Follicle stimulating hormone (FSH) in a concentration 100 ng ml-1 of culture medium did not influence significantly the androgen production.

Animals↗
PubMed1978

Serum testosterone and testicular response to HCG in young and aged male rats.

Serum testosterone and testicular response to HCG was measured in young (3 - 6 mo) and aged (20 - 30 mo) male Long-Evans rats. Serum testosterone was measured by radioimmunoassays on serial blood samples taken before and after injections of HCG. Control group serum testosterone concentrations were lower in aged compared to young groups. Intravenous injection of 1, 5, and 20 IU of HCG increased serum testosterone in both age groups and testosterone remained elevated throughout the 150-min sampling interval. The increase in serum testosterone concentrations following acute HCG stimulation was greater in young than in aged rats. Serum testosterone concentrations and testicular response to intravenous HCG injections were increased to similar levels in young and aged male rats following 7 days of daily subcutaneous injections of 5 IU of HCG/100 gm bw. These data suggest that while testicular secretion and responsiveness is reduced with age, the aged male rat retains the capacity to secrete more testosterone than it normally maintains.

Aging↗
PubMed1989

The blood vascular architecture of the rat testis: a scanning electron microscopic study of corrosion casts followed by light microscopy of tissue sections.

The blood vascular bed of the rat testis was studied by scanning electron microscopy (SEM) of corrosion casts and by light microscopy of tissue sections. The testicular artery penetrates the pampiniform plexus and gives rise to the intertubular arterioles. Each of these arterioles courses in the intertubular connective tissue column, and gives off intertubular and peritubular capillaries. The intertubular capillaries pass the intertubular connective tissue column, whereas the peritubular capillaries reach the peritubular connective tissue sheet. The intertubular and peritubular capillaries anastomose with each other and converge into the intertubular venules in the intertubular connective tissue columns. Thus, the blood vascular bed of the rat testis consists of hexago- or pentago-columnar capillary networks which commonly surround the seminiferous tubules. The Leidig's cells are preferentially observed in the intertubular connective tissue columns. One of the intertubular capillaries is consistently thick, and directly continues into the intertubular venules (arteriolo-venular capillary channels), which finally drain into the pampiniform plexus. These findings suggest that the male sex hormone, testosterone, as secreted by the Leidig's cells, is discharged into the intertubular capillaries and then mainly carried by the arteriolo-venular capillary channels and intertubular venules into the pampiniform plexus. This specialized drainage may ensure the presence of highly concentrated testosterone in the pampiniform plexus and allow the testosterone-exchange from the pamipiniform plexus to the testicular artery. The arteriolo-venular capillary channels may also eliminate blood congestion in the testis to enhance the efficiency of the heat-exchange mechanism between the testicular artery and pampiniform plexus. Many arterio-arterial and arterio-venous anastomoses occur, which may regulate the blood flow within the testis.

Animals↗
PubMed1981

Serum testosterone response in Holstein bulls after administration of luteinizing hormone.

Seven yearling Holstein bulls were given 0, 20, 40, 60, 80, 100 and 200 micrograms NIH-LH-B9 during a 7-day complete Latin square design experiment. Treatments were administered via jugular cannulas at 0900 hr, and blood was collected at 60, 30 and 0 min before treatment, at 15-min intervals for 3 hr after treatment and at 30-min intervals from 3 to 7 hr after treatment. Luteinizing hormone (LH) and testosterone concentrations wer measured in serum by radioimmunoassay. Area under the LH and testosterone response curves, expressed as nanograms per milliliter x hours, increased (P less than .001) with increasing amounts of exogenous LH. Basal LH in serum averaged 1.4 +/- .1 ng/ml, and peaks ranged from 3.8 +/- .4 to 13.3 +/- .4 ng/ml after 40 and 200 micrograms of exogenous LH, respectively. Basal testosterone in serum of bulls given saline was 1.8 +/- .2 ng/ml, and peak responses ranged from 4.1 +/- .3 ng/ml to 5.9 +/- .5 ng/ml after 40 and 200 micrograms exogenous LH, respectively. The LH area response to exogenous LH was linear (Y = .4717 + .0352X; P less than .001), with testosterone concentration reaching maximum level in response to 100 micrograms LH (Y = 1.0279 + .1041X + .0001X(2); P less than .001). On the basis of these data, we suggest that the magnitude of the pulsatile release of LH quantitatively controls the secretion of testosterone from the testes of yearling bulls.

Animals↗
PubMed1990

Gonadotropin-releasing hormone deficiency in men: diagnosis and treatment with exogenous gonadotropin-releasing hormone.

Idiopathic hypogonadotropic hypogonadism in men is the result of absent or abnormal secretion of gonadotropin-releasing hormone, which prevents pubertal development. Isolated gonadotropin-releasing hormone deficiency is clinically and neuroendocrinologically heterogeneous, largely because of variation in the degree of gonadotropin-releasing hormone deficiency. Treatment with pulsatile gonadotropin-releasing hormone results in normal pubertal changes and virilization. Such treatment has been uniformly successful in normalizing release of gonadotropins and secretion of testosterone. Improvement in secondary sex characteristics and induction of spermatogenesis have been achieved in most patients. Eight of nine patients desiring induction of fertility were able to father a child. Use of pulsatile gonadotropin-releasing hormone presents a powerful model in which to examine regulation of gonadotropin secretion and the role of hypothalamic gonadotropin-releasing hormone in control of the male reproductive axis.

Adolescent↗
PubMed1991

The control of testicular androgen production in the goldfish: effects of activators of different intracellular signalling pathways.

The putative roles of different signal transduction pathways in the regulation of testicular androgen production in goldfish were investigated. In addition to the role of the gonadotropin-adenylate cyclase pathway, which was studied using human chorionic gonadotropin and forskolin, we determined the effects of changes in intracellular calcium content and protein kinase C activation on androgen production using calcium ionophore A23187 and phorbol 12-myristate 13-acetate (PMA), respectively. Testis fragments incubated in vitro respond to hCG in a time- and dose-dependent manner with a resultant increase in the secretion of testosterone (T) and 11-ketotestosterone (11-KT). Although ineffective alone, PMA (400 nM) and A23187 (4000 nM) stimulate a small but significant increase (3-fold above basal) in T production. This response is minor compared to the up to 200-fold increase in T secretion observed in response to either hCG or forskolin. PMA (25-400 nM) alone and A23187 (250-4000 nM) alone inhibit the stimulatory actions of hCG on T production. Unlike PMA, the inactive phorbol 4 alpha-phorbol didecanoate, which does not activate PKC, had no effect on hCG-stimulated T production. PMA and A23187 did not influence the effects of forskolin on T production, suggesting that the compounds exert their effects prior to adenylate cyclase activation. In summary, the present studies suggest that in addition to the stimulatory actions of the adenylate cyclase second messenger system, changes in intracellular calcium content and protein kinase C activation may modulate testicular androgen production in the goldfish.

Animals↗
PubMed1978

Endocrine regulation of reproductive development and function in the male.

Sexual development is an ordered process that begins at the moment of fertilization and terminates with the production and transfer of viable gametes. The formation of the male gonad depends upon genes located on both sex chromosomes and autosomes. Differentiation and growth of the male reproductive system is directed by the fetal testis through the production of a putative peptide which causes the regression of the Mullerian ducts and the secretion of testosterone which virilizes the Wolffian duct and thereby directs the differentiation of the internal accessory structures of reproduction. A third hormone, dihydrotestosterone, is synthesized intracellularly from testosterone within the urogenital sinus and tubercle. The action of this hormone controls the formation of the prostate and the external genitalia characteristic of the male phenotype. The postnatal growth of the testis and accessory sex tissues follows a characteristic curvilinear pattern with the most prominent increments coincident with the onset in testosterone production. Spermatogonial differentiation may proceed in the absence of hypophyseal or gonadal hormones but the respective maturation divisions of primary and secondary spermatocytes and the completion of spermiogenesis are clearly dependent upon testicular steroids produced under the influence of LH. Germ cells differentiate in a unique environment created, in part, by the blood testis barrier which arises as a result of tight-junctional complexes formed between adjacent Sertoli cells. Sertoli cells actively secrete fluids and export an androgen binding protein under the influence of androgens and FSH. Maintenance of spermatogenesis depends on high intratubular concentrations of testosterone, provided in part by the steroidogenic actions of LH on the Leydig cell and, in part, by the production of androgen binding protein by the Sertoli cell. Thus, both gonadotropins act in concert to maintain germ cell production. Selective removal of either LH or FSH curtails sperm production but testosterone supplementation, in adequate amounts, allows spermatogenesis to proceed in the absence of the pituitary gland.

Androgens↗
PubMed2003

Testosterone-dependent effects of galanin on pituitary luteinizing hormone secretion in male rats.

Galanin is a 29-amino-acid peptide that colocalizes with GnRH in hypothalamic neurons. High concentrations of galanin are present in portal vessel blood of both male and female rats, and galanin receptors are present on gonadotropes in both sexes. Results from studies of female rats indicate that galanin acts at the level of the pituitary to directly stimulate LH secretion and also to enhance GnRH-stimulated LH secretion. The effects of galanin on pituitary LH secretion in male rats are relatively uncharacterized; thus, the present in vivo study was conducted 1). to examine the ability of galanin to affect basal or GnRH-stimulated LH secretion in male rats and 2). to determine whether the effects of galanin on LH secretion in male rats are testosterone-dependent. All three doses of galanin used (1, 5, and 10 micro g/pulse) significantly enhanced GnRH-stimulated LH secretion in intact male rats. Only the highest dose of galanin directly stimulated LH secretion (without GnRH coadministration) in intact males. Galanin did not directly stimulate LH secretion or enhance GnRH-stimulated LH secretion in castrated male rats. In fact, the highest dose of galanin inhibited GnRH-stimulated LH secretion in castrated males. Upon testosterone replacement, the ability of galanin to directly stimulate LH secretion and to enhance GnRH-stimulated LH secretion was restored in castrated males. These results suggest a role for galanin in the regulation of LH release in male rats and demonstrate that testosterone upregulates the ability of the pituitary to respond to the stimulatory effects of galanin.

Animals↗
PubMedDate not supplied

Effects of bismuth citrate on the viability and function of Leydig cells and testicular macrophages.

Bismuth is present in several popular over-the-counter drugs for nausea and diarrhea and is occasionally abused by patients with chronic gastrointestinal disorders. The most common consequence of bismuth overdose is neurological dysfunction. In experimental animals, bismuth overdose results in lowered serum testosterone levels, suggesting that reproductive dysfunction may be an additional component of bismuth toxicity. Although the precise mechanisms responsible for the lowered testosterone levels are unknown, it has been shown that bismuth accumulates within testicular macrophages. This may be important because these cells, which are commonly found in direct contact with Leydig cells, are known to exert paracrine influences on the Leydig cells for local control of testosterone production. However, bismuth may also exert direct effects on Leydig cells because it passes by these cells on its way to the phagocytic macrophages. The purpose of the present studies was to isolate both testicular macrophages and Leydig cells from rat testis and study the direct effects of bismuth on these cells with regard to their viability and function. We found that when Leydig cells were treated for 24 h with bismuth (1-100 microM) no change in viability or secretion of testosterone was observed. However, when testicular macrophages were similarly treated with bismuth a significant effect on viability was observed with as little as 6.25 microM bismuth, with near-complete cell death at 50 microM after 24 h. However, bismuth had no effect on the viability on testicular macrophages at 50 microM up to 8 h, therefore, we studied the secretion of tumor necrosis factor alpha (TNF-alpha) after 4 h of exposure to 50 microM bismuth and found no influence on the production of TNF-alpha. Taken together, it seems likely that bismuth has no direct effects on Leydig cells but, rather, lowers testosterone levels by killing testicular macrophages, thereby interrupting their local paracrine influence on Leydig cells through factors other than TNF-alpha.

Animals↗
PubMed1979

[Plasma testosterone, free testosterone fraction LH and FSH in males during the early stage of acute myocardial infarction (author's transl)].

In 18 males (age 49--79 yrs) without endocrine diseases, testosterone, free testosterone fraction, LH, FSH and cortisol (as indicator for stress) were determined in the early stage of an acute myocardia infarction. Blood was taken on admission as well as every 4 hours up to meanly 43 hours. The patients were separated in 2 groups for proving whether alterations of the parameters may depend on the severity of the myocardial infarction (group A=severe infarction; group B=not severe infarction). Testosterone showed a rapid decrease in the first 11 hours after admission, which continued less striking to the end of the investigation. Testosterone was significantly decreased in group A in comparison to group B. LH and FSH in both groups together were remarkably reduced during the whole time. Whereas group A demonstrated a tendency to decreased values in comparison to group B for LH, there were not any essential differences between the two groups for FSH. The free testosterone fraction was not altered. Cortisol in group A was twice as high as in group B during the entire investigation. The systolic pressure in group A was generally lower than in group B during the whole time. The results demonstrate an important reduction of the secretion of testosterone, LH and FSH during the early stage of the acute myocardial infarction. The testosterone suppression seems to be dependent on the severity of the myocardial infarction. These alterations may be caused by a general impaired perfusion as a consequence of myocardial infarction and a suppressive effect of increased cortisol values on testosterone levels.

Aged↗
PubMed1998

Variation in the end products of androgen biosynthesis and metabolism during postnatal differentiation of rat Leydig cells.

The amount of testosterone (T) secreted by Leydig cells is determined by a balance between T biosynthetic and metabolizing enzyme activities. It has been established that 5alpha-androstan-3alpha,17beta-diol (3alpha-DIOL) is the predominant androgen secreted by the testes of immature rats during days 20-40 postpartum, whereas T is the major androgen by day 56. However, the underlying changes in T biosynthetic and metabolizing enzymes during Leydig cell development and their magnitudes have remained unclear. The aim of the present study was to define the developmental trends for T biosynthetic and metabolizing enzymes in Leydig cells at three distinct stages of pubertal differentiation: mesenchymal-like progenitors on day 21, immature Leydig cells on day 35, and adult Leydig cells on day 90. Production rates for precursor androgen (androstenedione), T, and 5alpha-reduced androgens [androsterone (AO) and 3alpha-DIOL] were measured in progenitor, immature, and adult Leydig cells in spent medium after 3 h in vitro. Steady state messenger RNA (mRNA) levels and enzyme activities of biosynthetic and metabolizing enzymes were measured in fractions of freshly isolated cells at each of the three stages. Unexpectedly, progenitor cells produced significant amounts of androgen, with basal levels of total androgens (androstenedione, AO, T, and 3alpha-DIOL) 14 times higher than those of T alone. However, compared with immature and adult Leydig cells, the capacity for steroidogenesis was lower in progenitor cells, with a LH-stimulated production rate for total androgens of 84.33 +/- 8.74 ng/10(6) cells x 3 h (mean +/- SE) vs. 330.13 +/- 44.19 in immature Leydig cells and 523.23 +/- 67.29 in adult Leydig cells. The predominant androgen produced by progenitor, immature, and adult Leydig cells differed, with AO being released by progenitor cells (72.08 +/- 9.02% of total androgens), 3alpha-DIOL by immature Leydig cells (73.33 +/- 14.52%), and T by adult Leydig cells (74.38 +/- 14.73%). Further examination indicated that changes in the predominant androgen resulted from differential gene expression of T biosynthetic and metabolizing enzymes. Low levels of type III 17beta-hydroxysteroid dehydrogenase (17betaHSD) mRNA and enzyme activity were present in progenitor cells compared with immature and adult Leydig cells. In contrast, levels of type I 5alpha-reductase (5alphaR) and 3alpha-hydroxysteroid dehydrogenase (3alphaHSD) mRNA and enzyme activities were dramatically lower in adult Leydig cells compared with those in progenitor and immature Leydig cells. Several T biosynthetic enzymes attained equivalent levels in immature and adult Leydig cells, but T was rapidly metabolized in the former to 3alpha-DIOL by high 5alphaR and 3alphaHSD activities, which were greatly reduced in the latter. Therefore, declines in 5alphaR and 3alphaHSD activities are hypothesized to be a major cause of the ascendancy of T as the predominant androgen end product produced by adult Leydig cells. These results indicate that steroidogenic enzyme gene expression is not induced simultaneously, but through sequential changes in T biosynthetic and metabolizing enzyme activities, resulting in different androgen end products being secreted by Leydig cells during pubertal development.

Androgens↗
PubMed1995

A double blind, placebo controlled study of the effects of low dose testosterone undecanoate on the growth of small for age, prepubertal boys.

OBJECTIVE: To assess whether very low doses of testosterone can accelerate growth without an undue advance in bone age in prepubertal boys with constitutional delay of growth. SUBJECTS: 23 prepubertal boys aged 11-14 years with height at or below the third centile for chronological age. DESIGN: Randomised, double blind trial comparing oral testosterone undecanoate 20 mg once daily versus placebo for six months. The 18 months' observation period of each subject comprised a six month pretreatment period, followed by a six month treatment (testosterone undecanoate or placebo) period, and a six month period after termination of treatment. OUTCOME MEASURES: At intervals of six months standing and sitting height were measured. Bone age, pubertal stage, weight, and lean body mass were also determined. Growth hormone, luteinising hormone, and follicle stimulating hormone secretion and testosterone concentration were measured before, after, and six months after treatment. RESULTS: Boys taking testosterone undecanoate (n = 11) showed a significantly greater height velocity (mean (SEM) 5.84 (0.53) cm/year) and sitting height velocity (3.54 (0.57) cm/year) during treatment than the placebo treated boys (n = 12, height velocity = 3.38 (0.22) cm/year, sitting height velocity = 1.58 (0.19) cm/year. There were no significant differences between the groups regarding changes in growth hormone, gonadotrophins, testosterone, or dihydrotestosterone concentrations. Bone age was not advanced significantly more rapidly in either group. CONCLUSIONS: There is accelerated gain in height during six months of treatment with low dose testosterone undecanoate, without a significantly greater rise in bone age compared with controls. Testosterone undecanoate is a safe, well tolerated, and effective treatment in the management of constitutional delay of growth.

Adolescent↗
PubMed1994

Evidence that testosterone and follicular fluid do not interact in the control of FSH secretion in rams.

The hypothesis that testosterone and inhibin interact in the control of FSH secretion in rams was tested. Adult rams were castrated and were simultaneously given testosterone implants and 3-times daily sc injections of 0, 0.4, 0.8 or 1.6 ml charcoal-treated bovine follicular fluid (bFF). After 1 wk, the implants were removed, and the bFF injections continued as before. Blood samples were taken daily for mean LH, FSH and testosterone concentrations, and every 10 min for 12 h in the presence and in the absence of testosterone for assessment of pulsatile LH release. The bFF specifically inhibited FSH secretion from rat pituitary cells in culture. In the presence of testosterone, there were no main effects of bFF on mean plasma FSH or LH concentrations, nor were these values different from their pre-treatment means (P>0.05). Treatment with bFF did not affect LH pulse frequency or amplitude, but the number of rams showing LH pulses was reduced in the 0.8 and 1.6-ml dose groups (P<0.05). Removal of testosterone increased (P<0.05) both gonadotropins. In the absence of testosterone, no main effect of bFF on mean LH or FSH concentrations was observed, although the 1.6-ml dose suppressed the postcastration rise of both LH and FSH. These data suggest that inhibin does not interact with testosterone and that a physiological level of testosterone is sufficient for the regulation of FSH secretion in adult rams.

Journal Article↗
PubMed1990

Sex differences in serum luteinizing hormone and testosterone in the human neonate during the first few hours after birth.

Blood was obtained from human male and female neonates within a few minutes after birth, and at intervals thereafter for up to 21 h. Serum LH was substantially higher at birth for boys than girls. For most boys, serum LH fell precipitously during the next hour; serum LH remained low for the remainder of the period sampled in both boys and girls. In girls, serum testosterone was low at birth and remained low for at least 21 h. At birth, serum testosterone in boys was higher than for girls, increased dramatically during the first 3 h after birth, and remained elevated (2 to 3 times higher than for girls) between 3 and 12 h after birth. In newborn human males, a sudden discharge of hypophyseal LH appears to stimulate neonatal secretion of testosterone by the testes. The functional significance of this phenomenon remains to be determined.

Chorionic Gonadotropin↗