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PubMed1982

Age variation of the 24-hour mean plasma concentrations of androgens, estrogens, and gonadotropins in normal adult men.

The 24-h mean plasma concentrations of androgens (dihydrotestosterone and total and free testosterone), estrogens (estrone and estradiol), and gonadotropins (LH and FSH) were measured in 35 healthy men, aged 21-85 yr, who were rigorously screened to exclude factors known or suspected to alter endocrine function. The plasma total testosterone concentration showed a slow continuous decline with age, decreasing about 35% between 21 and 85 yr of age; the free testosterone level was closely correlated with that of total testosterone over the entire observed concentration range. The concentrations of dihydrotestosterone, estrone, estradiol, and LH were age invariant. The concentration of FSH showed a continuous linear increase with age; the level at age 85 was about 2.5 times the level at age 21. The following conclusions were drawn. 1) Testosterone secretion appears to decline slowly and continuously throughout adult life in men. 2) Measurement of the plasma free testosterone level adds no independent information in healthy men, since its level is closely correlated with that of total testosterone at all concentrations. 3) The continuous rise with age in FSH concentration while LH is age invariant cannot be explained by changes in testosterone or estrogen production, but might be due to a decline of inhibin production with age.

Adult↗
PubMed2005

[Culture and identification of human adult Leydig cells].

OBJECTIVE: To obtain a simple and effective method to isolate and purify adult Leydig cells. METHODS: The testes of human adults were digested and then the density gradient centrifugation of the cells was performed with four different Percoll concentrations (60%, 34%, 26%, 21%) to isolate Leydig cells, whose characteristics were identified by cytological observation staining, 3beta-HSD staining and detection of hCG and testosterone secretion. RESULTS: High-concentration (> 90%) purified Leydig cells were acquired, and many identification experiments demonstrated the adequate testosterone secretory function of the isolated and purified Leydig cells. CONCLUSION: This method is easy and efficient for the isolation and purification of adult Leydig cells.

Adult↗
PubMed1984

The modified method for isolation and culture of highly homogeneous Leydig cell population from rat testes.

A modified method for isolation and culture of a pure population of rat Leydig cells is described. For obtaining crude interstitial cell suspension, decapsulated testes were dispersed in 0.02% collagenase solution in Ca2+, Mg2+--free Hanks medium for 1 hour. Then, approx. 5 X 10(7) cells were centrifuged in 10-90% discontinuous, isoosmotic Percoll gradient at 3000 g for 20 min. The cells from eight fractions obtained were collected and cultured in Eagle's MEM for 4 days. Using morphological methods, 1.059-1.070 g/ml density fraction contained 97% and 1.070-1.080 g/ml fraction contained 90% viable Leydig cells. The cells secreted testosterone to the culture medium and responded to LH stimulation with over four-fold increase in hormone secretion.

Animals↗
PubMed1997

Effects of acute hyperinsulinemia on testosterone serum concentrations in adult obese and normal-weight men.

In a previous study performed in adult obese and normal-weight male subjects, we found that suppression of insulin levels by diazoxide reduced testosterone and increased sex hormone-binding globulin (SHBG) blood concentrations. These and other data suggested that insulin may have a regulatory capacity in testosterone secretion and/or metabolism in men, similar to what has already been demonstrated in women. In this study, we investigated the effects of acute hyperinsulinemia on major androgen levels, including testosterone, in two groups of normal-weight in = 11) and obese (n = 9) men. Acute hyperinsulinemia was obtained by the euglycemic-hyperinsulinemic clamp technique. Relationships between the degree of insulin resistance (ie, total glucose disposal [M value]) and testosterone levels were also evaluated. Basal testosterone levels in obese subjects (10.40 +/- 3.02 nmol/L) were significantly lower than in normal-weight controls (15.50 +/- 4.65 nmol/L, P < .01), whereas no difference was present in androstenedione and dehydroepiandrosterone sulfate (DHEA-S) concentrations. During the clamp study, testosterone was significantly increased in the obese group (11.79 +/- 3.64 nmol/L, P < .05) but not in the control group (15.81 +/- 4.54 nmol/L, P = NS). The other two androgens did not significantly change in either the obese or control group. There was a highly significant correlation between baseline testosterone concentrations, with M values suggesting a relationship between impaired peripheral insulin sensitivity and reduced plasma testosterone concentrations. It should be pointed out that there was a certain discrepancy in the testosterone variations, particularly in the control group, in which two thirds of the subjects had no change or some decrease in testosterone levels, whereas in the remainder testosterone increased over the values of the assay variation coefficient. These findings are consistent with the hypothesis that insulin may regulate testosterone blood levels also in male subjects. Whether these effects are primarily due to increased hormone secretion or reduced clearance needs to be investigated.

Acute Disease↗
PubMed1993

Modulation of reproductive hormone secretion by nutritional intake: stress signals versus metabolic signals.

States of chronic undernutrition can cause a profound suppression of reproductive function. To begin to determine the time course and the nature of the mechanism by which undernutrition suppresses the activity of the reproductive axis we have examined the effects of brief periods of fasting on reproductive hormone secretion in men and male rhesus monkeys. In monkeys there is a significant suppression of pulsatile luteinizing hormone (LH) and testosterone secretion after a single day of fasting, that is apparent within the first 4 h after a meal is missed. The suppression of pulsatile LH secretion on a day of fasting does not appear to be caused by the psychological stress experienced when monkeys are deprived of their daily meal in that monkeys who are maintained in a metabolically fed state (by feeding a large excess of food on the day prior to fasting), but are deprived of a meal and displayed behavioural agitation associated with fasting, have no suppression of LH secretion. The suppression of LH secretion on a day of fasting cannot be reversed by naloxone infusion, indicating that increased secretion of opioid peptides is not the primary mechanism causing the decrease in the central drive to the reproductive axis during fasting.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Increase in Leydig cell responsiveness in the unilaterally cryptorchid rat testis and its relationship to the intratesticular levels of testosterone.

Adult rats were made unilaterally cryptorchid (UCD) and 6-7 weeks later Leydig cells were isolated from the scrotal and abdominal testes and their capacity to secrete testosterone in vitro was compared. Basal testosterone production by Leydig cells from the abdominal testes of UCD rats was lowered, compared with cells from the contralateral scrotal testes, whilst their responsiveness to both human chorionic gonadotrophin and an LH releasing hormone agonist was enhanced two- to threefold (P less than 0.001) compared both with cells from the contralateral scrotal testes and with cells isolated from untreated rats of the same age. In the UCD rats, concentrations of testosterone in testicular interstitial fluid (IF) were reduced (P less than 0.001) by 70-90% in abdominal, compared with scrotal, testes. A similar reduction was evident in the levels of testosterone in spermatic venous blood, and both this decrease and that in IF levels of testosterone varied according to the degree of testicular involution. The ontogeny of the above changes was investigated. After induction of unilateral cryptorchidism, the weight of the abdominal compared with the scrotal testis declined slowly, such that by day 5 there was only a 25% reduction in weight compared with a 70% reduction by day 40. In contrast, the levels of testosterone in IF from abdominal testes declined rapidly, such that by day 5 an 80% reduction was attained, compared with scrotal testes, with little further change by day 40.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Chlordecone lacks estrogenic properties in the male rat.

The reproductive toxicity of chlordecone has been hypothesized to derive from estrogen mimicry. To test this hypothesis, the effects of estradiol-17 beta, testosterone, and chlordecone on the male reproductive tract of 60-day-old male rats were compared after 72 days of exposure. Estradiol-17 beta (25 micrograms/week) and testosterone (945 micrograms/week), administered by polydimethylsiloxane capsules implanted subdermally, caused significant reductions in spermatogenesis, sperm motility, testicular capacity for secreting testosterone, and the weights of testes and epididymides. Estradiol-17 beta also caused significant declines in serum testosterone concentrations, and the weight of the prostate and seminal vesicles. Chlordecone, administered either by polydimethylsiloxane capsule or by ip injection, had no effect on any of these parameters, except to reduce significantly seminal vesicle weight at the highest dose of injected chlordecone, 7.5 mg/week. Therefore, chlordecone does not mimic estrogen in its effects on the reproductive system of the male rat.

Animals↗
PubMed1996

Evidence that heparin binding autocrine factors modulate testosterone production by the adult rat Leydig cell.

Androgen production by adult rat Leydig cells is stimulated by pituitary LH but can also be modulated in vitro by paracrine stimulatory and inhibitory factors, many of which belong to growth factor families. Their actions are mediated through cell surface or extracellular matrix proteoglycans and the aim of this study was to determine the role of cell surface heparan sulfate proteoglycans in the regulation of testosterone secretion by adult rat Leydig cells. The presence of sodium chlorate (25 mM) and protamine sulfate (10 micrograms/ml) inhibited testosterone production by LH stimulated cells by over 50%, but had no effect on unstimulated cells. The LH responsiveness and testosterone production returned to normal after these agents were removed from the culture media. No significant difference in LH receptor numbers at the end of the culture period was seen between sodium chlorate treated and untreated cells. Testosterone production by dibutryl-cAMP stimulated Leydig cells was also inhibited by sodium chlorate. The addition of heparin inhibited testosterone production by LH stimulated cells in a dose-dependent manner, however, in unstimulated Leydig cells heparin stimulated testosterone production to up to 50% of that seen in LH stimulated cells. These data suggest that cell surface heparan sulfate proteoglycans modulate testosterone production by adult Leydig cells in vitro, and that this may involve the autocrine actions of heparin binding growth factors on the Leydig cells.

Animals↗
PubMed1984

Anterior pituitary hormonal regulation of testicular gonadotropin-releasing hormone receptors.

Testicular GnRH receptors are increased 2-fold 1 day after hypophysectomy and remain elevated for up to 6 days. Consequently, the present study was undertaken to determine which pituitary hormone(s) regulated testicular GnRH receptors. Adult male rats were hypophysectomized and injected sc every 8 h for 2 days with LH, FSH, GH, PRL, estradiol, testosterone, 5 alpha-dihydrotestosterone, and vehicle (controls), beginning within 5 h of surgery. The animals were decapitated on the third day after hypophysectomy, the testes were excised, and interstitial tissue was teased from seminiferous tubules before storage at -70 C until assayed. The analog D-Ala6-des-Gly10-GnRH ethylamide was used to assess GnRH receptors on 10,800 X g-membrane fractions of interstitial tissue. The administration of GH, PRL, and FSH at concentrations which maintained LH receptors in adult or immature hypophysectomized rats did not prevent the increase in GnRH receptors, whereas LH replacement prevented the rise in GnRH analog binding in a dose related manner. LH also reduced preexisting posthypophysectomy increases in GnRH receptor concentrations. Injections of estradiol (5 micrograms/day) partially inhibited the posthypophysectomy increase in GnRH receptors, whereas the androgens 5 alpha-dihydrotestosterone and testosterone were ineffective. These results indicate that LH can regulate testicular GnRH receptors. Since GnRH directly inhibits testosterone secretion, inhibition of testicular GnRH receptors by LH may be one of the mechanisms by which LH replacement enhances testosterone production after hypophysectomy.

Animals↗
PubMed1996

Effects of selenium deficiency on testicular morphology and function in rats.

For four generations rats were fed a low selenium diet (2-7 micrograms Se kg-1) or the same diet with 250 or 300 micrograms Se kg-1 added as selenite. In male rats of the first generation that had been fed the diets from the age of 20 days onwards, selenium depletion led to slightly delayed testis growth during pubertal development that was compensated for in the later stages of maturation. In adult rats fed the low selenium diet for nearly a year no changes in testicular mass and morphology were observed. The serum concentration of testosterone of 6-month-old, selenium-depleted animals was, however, slightly lower than that of adequately supplied controls, and the stimulation of testosterone secretion by administration of GnRH or LH resulted in a significantly less marked rise in the serum concentration of testosterone. From the second generation onwards the testis mass, expressed as a percentage of the body mass, decreased and in the fourth generation was less than 50% of that of the controls. The male gonads of fourth generation animals showed a severe bilateral atrophy, in which the seminiferous tubules were considerably reduced in diameter and almost entirely lined by Sertoli cells and a few stem cells. Differentiated spermatozoa could not be detected. The alterations were reversible and spermatogenesis was restored by feeding the selenium-adequate diet. The findings indicate that testicular morphology and functions are affected by severe selenium deficiency and that the element is necessary for testosterone biosynthesis and the formation and normal development of spermatozoa.

Animals↗
PubMed1981

The treatment of essential hirsutism in women with cyproterone acetate and ethinyl estradiol. Clinical and endocrine effects in 10 cases.

Ten women with essential hirsutism were treated for one year with cyclic administration of cyproterone acetate and ethinyl estradiol. Biochemical and clinical control took place after 1, 3, 6 and 12 months of treatment. In 4 patients great improvement of hirsutism was noted, but only after 6 months of therapy. In 4 patients there was some improvement, while 2 were resistant. Side effects included reduced libido in 4 cases, mental depression in 3, dry skin and itching in 4 and transient nausea in one, but never necessitated cessation or interruption of treatment. Several changes in endocrine function took place during treatment: testosterone secretion rate diminished together with the urinary excretion of 17-KS and 17-KGS, while the serum concentration of testosterone binding globulin increased. There was a reduction in the serum concentration of total endogenous estrogens and progesterone as well as LH. No changes in hepatic, renal or hematologic parameters were found except for a slight increase in plasma prothrombin time. Clinical outcome of therapy could not be correlated with a pretreatment endocrine "profile", nor with the changes that this therapy induced in endocrine function. It is concluded that the anti-androgenic effect is probably the most important in this drug regimen, but that reversibility of hirsutism may depend upon factors not directly related to androgen influence.

17-Hydroxycorticosteroids↗
PubMed1981

[Investigations on the genesis of the pubertal growth spurt (author's transl)].

The pubertal growth spurt is based on synergistic effects of hGH and androgenic steroids. It fails to appear in androgen deficiency as well as in complete absence of hGH. Apart from the synergism of biological functions there are interactions with regard to the secretion of hGH and androgens. Investigating the nocturnal hGH-secretion in puberty stage 3 we found twice as high secretion rates as in stage 1. Children with anorchia or constitutional delay of growth and adolescence during treatment with testosterone secreted more than threefold amounts of hGH as before. In two cyproterone acetate-treated adolescents, and in four 12-19 years old patients with hypogonadism, the nocturnal secretion rates of hGH as well as the maximal hGH-peaks attained were lower than in normal prepubertal children. The conclusion is drawn that the androgen-secretion during adolescence is not only prerequisite to the hGH-increment necessary for the pubertal growth spurt but also to the preservation of basal hGH-secretion.

Adolescent↗
PubMedDate not supplied

Endocrine function of the postmenopausal ovary.

The ovaries of postmenopausal women are smaller than those of premenopausal women and consist primarily of stromal cells. These cells have receptors for, and respond to, gonadotropins and secrete testosterone and lesser amounts of other androgens and estrogens. The ovaries of some postmenopausal women contain P-450 aromatase and secrete estradiol. There is little evidence that inhibins A or B are secreted by postmenopausal ovaries.

Androgens↗
PubMed1990

Gonadotrophin-releasing hormone and human chorionic gonadotrophin tests reveal that both hypothalamic and testicular endocrine functions are suppressed during acute prolonged physical exercise.

The mechanism of suppression of gonadotrophins and testosterone during prolonged exercise was studied. Fourteen healthy males were injected immediately before an exhaustive bicycle run for 4 h, and before a control period without exercise, with one of the following substances: (1) 1 ml of saline, (2) 100 micrograms of a GnRH agonist (buserelin), and (3) 50 IU/kg of hCG. Each test was repeated for each subject 2 weeks apart, in a randomized single-blind fashion. Blood samples were taken before the injections (sample A), 6 h after the injections (sample B), and the following morning (sample C). During placebo treatment testosterone concentration decreased from A samples to B samples more in the exercise trial than in rest trial (31 vs 8%, P = 0.02). This exercise-associated decrease was reversed by both the GnRH agonist and hCG treatments. Serum gonadotrophin concentrations responded identically to GnRH agonist injections during exercise and rest trials. hCG resulted in a greater increase of serum testosterone from A to C samples at rest than during the exercise trial (52 vs 33%, P = 0.04). In conclusion, the exercise-induced suppression of serum testosterone is associated with two effects: suppressed endogenous GnRH stimulation of gonadotrophin release during exercise, and decreased testicular capacity to secrete testosterone during recovery period.

Adult↗
PubMed1984

The pure antiandrogen RU 23908 (Anandron), a candidate of choice for the combined antihormonal treatment of prostatic cancer: a review.

The nonsteroidal antiandrogen RU 23908 ( Anandron ) weakly interacts with the prostatic cytosolic androgen receptor and shows a fast dissociation rate. When administered to immature castrated rats up to the daily dose of 100 mg/kg, it is devoid of any androgenic activity but efficiently blocks the growth-promoting activity of androgens on ventral prostate and seminal vesicle weight, thus showing the characteristics of a pure antiandrogen. In intact animals, on the other hand, the antiandrogen administered alone exerts only a partial inhibition of prostate and seminal vesicle weight. This is due to the property of the pure antiandrogen to neutralize the inhibitory feedback effect of androgens at the pituitary level on the LH responsiveness to LHRH, as illustrated in vitro in rat anterior pituitary cells in culture as well as in vivo in intact and castrated animals. In intact animals, neutralization of the inhibitory feedback action of endogenous androgens leads to an increased LH and testosterone secretion, which partly overcomes the direct action of the antiandrogen at the level of the prostate and seminal vesicles. In fact, the plasma testosterone concentration is more than doubled 6 hr after the administration of 10 mg of RU 23908 while plasma LH and testosterone levels are increased by 7- and 17-fold, respectively, after 14 days of similar daily treatment. Efficient neutralization of the androgenic action at the prostatic level in intact animals thus requires prevention of this escape phenomenon through inhibition of LH secretion. Although inhibition of LH release can be achieved by estrogen and progestins, an optimal inhibitory effect on the prostate is obtained by the combined administration of the antiandrogen with an LHRH agonist that causes a specific blockage of testicular androgen biosynthesis as well as an inhibition of the LH responsiveness to LHRH.

Androgen Antagonists↗
PubMed1980

Effects of a prolactin-secreting pituitary tumor on hypothalamic, gonadotropic and testicular function in male rats.

The presence of a transplanted prolactin- and GH-secreting pituitary tumor (Furth MtT.215) in inbred male rats resulted in increased hypothalamic LHRH and pituitary LH content, decreased serum LH and testosterone concentrations, and very high serum prolactin values. The pituitary tumor also inhibited LH release by the in situ pituitary in response to orchidectomy, or orchidectomy, or adrenalectomy, and reduced the LH response to LHRH administration. Testes weight was significantly reduced and adrenal weight was significantly increased in the rats carrying pituitary tumors. These results that inhibitory effects of the transplanted pituitary tumor on LH and testosterone secretion were affected both a reduction in hypothalamic LHRH release and a reduced responsiveness of the pituitary to LHRH.

Adrenalectomy↗
PubMed1975

Stimulation of testosterone production by isolated rabbit ovarian follicles in the presence of luteinizing hormone and phenylmethylsulfonyl fluoride.

Luteinizing hormone (LH) causes a dramatic increase in steroidogenesis by isolated rabbit follicles which secrete testosterone as a major product. In order to determine whether the source of this testosterone could be from stores of cholesterol esters rabbit follicles were incubated with LH and phenylmethylsulfonyl fluoride (PMSF) an inhibitor of cholesterol esterase. No inhibition of testosterone production could be detected in the presence of PMSF indicating that cholesterol esters are not precursors for testosterone synthesis by rabbit follicles.

Animals↗
PubMed1989

Stimulation of Sertoli cell inhibin secretion by the testicular paracrine factor PModS.

The testicular paracrine factor PModS is produced by peritubular myoid cells under androgen control and modulates Sertoli cell function and differentiation. The observation that luteinizing hormone (LH) stimulates inhibin production in vivo, but has no effect on isolated Sertoli cells in vitro, suggested an indirect mode of LH action, potentially mediated by PModS. The effects of the testicular paracrine factor PModS and hormones on inhibin secretion by Sertoli cells were investigated to provide insight into the endocrine control of inhibin expression. An inhibin radioimmunoassay was utilized which showed essentially parallel displacement curves with purified bovine follicular fluid inhibin, Sertoli cell conditioned medium and concentrated Sertoli cell secreted proteins. An immunoblot analysis of Sertoli cell secreted proteins with the inhibin antisera consistently detected a 32 kDa protein which is the expected size of the mature of inhibin (alpha beta) and periodically detected a 57 kDa protein which is speculated to be an incomplete processed form of the inhibin precursor (alpha 43 beta). Follicle-stimulating hormone (FSH) was found to stimulate inhibin secretion initially between days 2 and 5 of Sertoli cell culture. Insulin and retinol alone had no significant effect on inhibin secretion; however, together they appeared to enhance the ability of FSH to stimulate inhibin secretion. Testosterone had no effect on inhibin production alone or in combination with other regulatory agents. PModS was found to stimulate inhibin secretion approximately 3-fold, but with a delayed time course of stimulation which did not occur until days 5-7 of Sertoli cell culture. Treatment with a combination of PModS and FSH resulted in an apparent maximal stimulation of inhibin secretion. Both forms of PModS, PModS (A) and PModS (B), were found to have equivalent biological activities in their ability to stimulate inhibin production with an apparent half-maximal effective concentration between 10 and 15 ng/ml. The current study provides evidence for the local testicular control of inhibin production and adds to the complexity of the endocrine control of inhibin expression. The cellular interaction is proposed in which LH acts on Leydig cells to stimulate androgen production which in turn acts on peritubular cells to regulate PModS production which subsequently can act on Sertoli cells to control inhibin production. Testicular control of inhibin production provides a potential short feedback loop for the local regulation of androgen production and an additional regulatory element for the pituitary-gonadal axis.

Animals↗