SEARCH · PubMed Health

Results for “testosterone”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,081 records · Page 60Linked to original sources

PubMed1994

Administration of testosterone during the follicular phase increased the number of corpora lutea in gilts.

The effects of 0 (vehicle), 1, 10, or 100 mg of testosterone, administered on d 17 and 18 of the estrous cycle (d 0 = 1st d of estrus), on the number of preovulatory follicles on d 19 or the number of corpora lutea (CL) and blastocysts on d 11 of the subsequent cycle were examined in 82 gilts. The mean number of preovulatory follicles increased (P < .01) in a dose-dependent manner. Likewise, gilts that received 1, 10, or 100 mg of testosterone had more (P < .05) CL than gilts treated with vehicle. The mean number of blastocysts increased (P = .06) in gilts receiving 1 mg of testosterone but decreased (P < .05) in gilts treated with 10 mg of testosterone compared with gilts receiving vehicle. Similarly, recovery rates of blastocysts decreased (P < .05) in gilts treated with 10 or 100 mg of testosterone relative to gilts administered 0 or 1 mg of testosterone. Plasma concentrations of testosterone and estradiol increased (P < .05) 2 h following administration of 1 mg of testosterone on d 17 of the estrous cycle. These results indicate that although the 10- and 100-mg dosages of testosterone were detrimental to blastocyst survival, the 1-mg dosage increased synthesis of estradiol and the number of CL and d-11 blastocysts.

Animals↗

PubMed1996

Effects of porcine somatotropin on circulating testosterone concentrations in boars and mechanism of action.

Four experiments were conducted to elucidate the effects of porcine somatotropin (pST, growth hormone) on circulating testosterone concentrations in boars. In Exp. 1, jugular-cannulated obese boars were administered 4 mg recombinant (r) pST/d for 24 d before collection of samples at 15-min intervals over 6 h for measurement of pST, testosterone, and LH. Somatotropin treatment decreased plasma concentrations of testosterone and LH (P < .05). In Exp. 2, White composite boars were administered rpST with implants (4 mg/d) for 10 to 28, 16 to 28, or 22 to 28 wk of age. Reductions in testosterone concentrations were proportional to the length of time rpST was administered; boars treated for 18 wk had the lowest testosterone concentrations. Concentrations of LH declined throughout the study in rpST-implanted boars but remained static in untreated, control boars. In vitro production of testosterone and dehydroepiandrosterone/dehydroepiandrosterone sulfate was unaffected by rpST treatment, and hCG stimulation of in vitro androgen secretion was similar in rpST and control treatments. In Exp. 3, i.v. injection of pituitary pST (USDA-B1; 5 micrograms/kg BW) into jugular-cannulated White composite and Meishan boars resulted in an acute increase in circulating LH followed by an increase in testosterone concentrations, which then declined to below preinjection levels at 6 to 7 h after pST injection. Multiple injections, two or four per day, of 5 micrograms pST/kg BW resulted in decreased testosterone concentrations in White composite boars, whereas in Meishan boars testosterone concentrations were unaffected (Exp. 4). Concentrations of LH were not different from control values in either breed, but in both breeds, four injections of pST per day produced lower LH concentrations than did two injections per day (P < .01). Depression of circulating concentrations of androgens in boars requires extended periods of pST treatment.

Animals↗

PubMed1997

Administration of testosterone from day 13 of the estrous cycle to estrus increased the number of corpora lutea and conceptus survival in gilts.

The effects of exogenous androgens on the number of corporea lutea (CL) and conceptus survival were examined in crossbred gilts. In Exp. 1, gilts received 1 mg of testosterone per day from d 13 (d = 0 first day of estrus, n = 21) or d 16 until estrus (n = 23). Gilts in the vehicle group received corn oil (n = 20). Gilts were mated and on d 11.5 their concepti and CL were evaluated. In Exp. 2, conceptus survival was examined at the 4- to 8-cell, early blastocyst or hatching blastocyst stages for gilts given vehicle or 1 mg testosterone from d 13 (24 gilts per group). In Exp. 3, gilts received 1 mg of androstenedione (n = 20) or vehicle (n = 18) per day from 13 d to estrus and then were mated and evaluated on d 11.5. Results from Exp. 1 indicated that the number of CL was greater (P < .04) in gilts treated with testosterone from d 13 to estrus than in gilts receiving vehicle (16.4 vs 14.8, respectively). Similarly, the number (P < .01) and recovery rate (P < .04) of blastocysts were greater in gilts treated with testosterone from d 13 to estrus than in gilts treated with testosterone from d 16 to estrus in gilts receiving vehicle (number, 15.3 vs 12.8 or 12.8; recovery rate, 95 vs 87 or 86%, respectively). Gilts treated testosterone or vehicle did not exhibit differences (P > .05) in number of normal concepti at the 4- to 8-cell and hatching stages. However, prior treatment with testosterone delayed conceptus death; gilts treated with testosterone had more (P < .01) normal concepti at the intermediate stage (early blastocyst) than those treated with vehicle (treatment x embryo stage interaction, P < .05). In Exp. 3, androstenedione treatment did not influence (P > .10) the number of CL or the number and recovery rates of d-11.5 blastocysts. Treating gilts with testosterone from d 13 of the estrous cycle to the following estrus increased the number of CL and blastocyst survival, perhaps by improving some, as yet unknown, aspect(s) of oocyte quality.

Androstenedione↗

PubMed1980

Testosterone regulation of luteinizing hormone and follicle stimulating hormone secretion in young male lambs.

Polydimethylsiloxane (Silastic) capsules containing crystalline testosterone were implanted subcutaneously in castrate lambs and evaluated for their ability to (1) provide stable, physiological concentrations of serum testosterone and (2) regulate secretion of LH and FSH. Testosterone was nondectable (< .2 ng/ml) between 12 and 24 weeks of age in the serum of castrate lambs implanted with empty capsules but was increased at those ages in lambs implanted with 20 cm (1.2 +/- .1 and .5 +/- .1 ng/ml), 60 cm (2.8 +/- .1 and .9 +/- .1 ng/ml) and 180 cm (6.6 +/- .3 and 1.9 +/- .2 ng/ml) of testosterone-filed Silastic tubing. Serum concentrations of LH and FSH were suppressed by exogenous testosterone and did not exceed concentrations in intact control rams as long as serum testosterone concentrations were greater than 1 ng/ml. In conclusion, simultaneous suppression of serum LH and FSH by concentrations of testosterone that cause a dose-dependent stimulatory effect on accessory sex gland weights indicates that testosterone is a physiological regulator of gonadotropin secretion in ram lambs. Although testosterone per se may not be directly responsible for negative feedback on LH and FSH secretion, the results presented herein question the need for a nonsteroidal "inhibin-like" testicular hormone to regulate FSH in lambs.

Animals↗

PubMedDate not supplied

The relationship between serum testosterone and visuomotor learning in hand skill in right-handed young women.

The relationship between serum testosterone level and motor learning in hand skill was studied in right-handed young women. Hand skill was assessed by a peg moving task. Subjects were required to shift 25 pegs from one of two parallel rows to the corresponding holes as fast as possible, first with right and then with left hand. One trial consisted of the time elapsed to move 25 pegs with one hand. Ten trials were performed by each hand. Peg moving times for the right and left hands linearly decreased at each successive trial (visuomotor learning). Subjects were divided into two subgroups as those having serum testosterone concentrations below and above the mean. The right hand skill and its motor learning was found to be better in subjects with low testosterone than those with high testosterone. The left hand skill was better in subjects with low testosterone than those with high testosterone; there was no significant difference in the left-hand learning in subjects with low and high testosterone (parallel regression lines). Motor learning linearly decreased with testosterone for the right hand, not for the left hand. These results seem to be in accord with the testosterone theory of cerebral lateralization (Geschwind & Behan, 1982).

Adolescent↗

PubMed1987

Modulation of prolactin responses to gonadotropin releasing hormone by acute testosterone infusions in normal women.

The administration of gonadotropin releasing hormone (GnRH) has been shown to stimulate prolactin (PRL), suggesting its role as an inducer of PRL release. This study addresses whether testosterone may modulate the release of PRL with GnRH during the early follicular phase when this stimulatory effect is not usually observed. Chromatographically pure testosterone was administered intravenously to 13 women in 2 doses (100 micrograms and 1000 micrograms) over a 6-hour period. GnRH (100 micrograms) was administered as a bolus 2 hours before and 4 hours after beginning testosterone. In addition, 3 women received testosterone twice, 3 months apart, with testolactone pretreatment on the second occasion. Serum testosterone rose in all patients and achieved maximum steady-state levels by 120 minutes. Serum estradiol (E2) was increased in subjects receiving the larger dose of testosterone but was unchanged with the lower dose and with the addition of testolactone. PRL did not increase significantly after GnRH before testosterone infusion but showed a significant increase after testosterone as well as after testosterone with testolactone. This effect did not appear to be dose-related.

Adolescent↗

PubMed1992

Inhibition of growth in chickens by testosterone, 5 alpha-dihydrotestosterone, and 19-nortestosterone.

The growth response of poultry to androgens is ambiguous, with both increases and decreases being reported. This may reflect the use of pharmacological doses. The present study examined the effect of physiological concentrations of androgens on growth of intact male, intact female, and castrated chickens. Physiological concentrations of androgen were attained by subcutaneous silastic implants. In mammals, androgens have both androgenic effects on the reproductive organs and anabolic growth-promoting effects on body and muscle growth. Some androgens, for instance 5 alpha-dihydrotestosterone (5 alpha-DHT) have high androgenic activity (5 alpha-DHT greater than testosterone) but others, e.g., 19-nortestosterone, have high anabolic activities (19-nortestosterone greater than testosterone greater than 5 alpha-DHT). The relative effects of testosterone, 5 alpha-DHT, and 19-nortestosterone on growth were compared in chickens. In young, intact male and female chicks, growth was suppressed by 1.0-cm silastic implants of testosterone and 5 alpha-DHT (5 alpha-DHT greater than testosterone). Castrated chicks were implanted with implants of various sizes (.3, 1.0, and 3.0 cm) containing testosterone, 5 alpha-DHT, or 19-nortestosterone. The androgens inhibited body weight gain: 19-nortestosterone reducing body weight at all three doses, 5 alpha-DHT reducing body weight at the intermediate and high doses, and testosterone tending to reduce body weight only at the high dose. Testosterone (3.0 cm), 5 alpha-DHT (all doses), and 19-nortestosterone (all doses) reduces skeletal growth, as indicated by shank-toe length. In contrast to their growth-suppressing effect, all three steroids exerted an androgenic effect; stimulating comb and wattle development (19-nortestosterone greater than 5 alpha-DHT greater than testosterone). It is concluded that androgens are androgenic but are not anabolic in chickens.

Adipose Tissue↗

PubMed2000

Association between plasma testosterone and work-related neck and shoulder disorders among female workers.

OBJECTIVES: The aims were to study the association between anabolic hormone testosterone in plasma and the presence of musculoskeletal disorders among female workers and to study the association between changes in testosterone and changes in musculoskeletal complaints. METHODS: In a cross-sectional design 145 women from 2 different industries filled out questionnaires about current musculoskeletal complaints, participated in a clinical examination of the neck and upper extremities, and gave a blood sample for the analysis of free testosterone in plasma. Individual characteristics, psychosocial job factors, and stress reactions were evaluated by questionnaires. In a follow-up study a subgroup of 73 sewing machine operators from the cross-sectional study was reexamined after 1 year. RESULTS: The group of women with clinically verified neck or shoulder disorders had significantly lower plasma testosterone than the women with no disorders. Furthermore, the testosterone level showed a negative association with age and a positive association with smoking and body mass index. Changes in pain status or clinically diagnosed musculoskeletal disorders were not associated with changes in testosterone levels. However, this finding may well be due to a strong plant influence in that marked changes in testosterone levels were observed for 2 of the 3 participating plants. CONCLUSIONS: There is some indication of an association between musculoskeletal disorders in the neck and shoulders and a low level of free plasma testosterone. The study failed to clarify the associations found between changes in testosterone and changes in musculoskeletal complaints over time.

Adult↗

PubMedDate not supplied

Testosterone-dependent restoration of spermatogenesis in adult rats is impaired by a 5alpha-reductase inhibitor.

Germ cell development (spermiogenesis in particular) in the adult rat is known to be testosterone dependent. Recently we proposed a role for the 5alpha reduction of testosterone to dihydrotestosterone (DHT) in the short-term restoration of round spermatid maturation when testicular testosterone levels are experimentally lowered. The current study aimed to further characterize the involvement of 5alpha-reductase in the restoration of spermatogenesis by investigating the short- and long-term restoration of specific germ cell populations by testosterone in the presence or absence of a 5alpha-reductase inhibitor (L685,273). Spermatogenesis in adult rats was suppressed for 8 weeks using 3-cm testosterone and 0.4-cm estradiol silastic implants (testosterone-estradiol [TE] treatment); spermatogenesis was then restored by administration of increasing doses of testosterone with or without a competitive 5alpha-reductase inhibitor or with the androgen receptor antagonist flutamide. Animals were then killed after either 4 days or 6 weeks of treatment so that we could study the short- and long-term restorations of spermatogenesis. Stereological analysis showed that germ cell development between late pachytene spermatocytes to round spermatids in stage VII during either short- or long-term restoration was not affected by 5alpha-reductase inhibition, but it was affected by flutamide. The conversion of round spermatids between stages VII and VIII was restored by testosterone treatment, but this restoration was prevented by flutamide. Both the short- and long-term restorations of this midspermiogenic event were significantly decreased when 5alpha-reductase was inhibited. After long-term restoration of spermatogenesis, elongated spermatids were restored to 42% of control but were significantly suppressed to 20% of control by coadministration of the 5alpha-reductase inhibitor because of a reduction in the number of round spermatids progressing between stages VII and VIII. The results demonstrate that the 5alpha-reduction of testosterone is particularly important for progression through midspermiogenesis, because this phase of germ cell development is more sensitive to withdrawal of androgens. We suggest that testicular 5alpha-reductase activity is important for the restoration or maintenance of low levels of sperm production in a hormonally based contraceptive setting.

5-alpha Reductase Inhibitors↗

PubMed2000

A prospective analysis of time to normalization of serum testosterone after withdrawal of androgen deprivation therapy.

PURPOSE: Patients with prostate cancer are treated with neoadjuvant, adjuvant and intermittent androgen deprivation therapy. Prostate specific antigen (PSA) is altered during androgen deprivation therapy, and as a result the prognostic significance and accuracy of PSA values measured before serum testosterone has normalized are questionable because the patient is still effectively on androgen deprivation therapy. We determine the time it takes for serum testosterone to return to normal after withdrawal of androgen deprivation therapy. MATERIALS AND METHODS: Serial serum testosterone was prospectively measured at 3-month intervals in 68 men after withdrawal of androgen deprivation therapy. The number of months to return to normal serum testosterone 270 ng./dl. or greater, was calculated for each patient. Patients were stratified according to duration of androgen deprivation, age and type of luteinizing hormone releasing hormone agonist used. RESULTS: Median patient age was 71 years (range 46 to 88). Median time to normalization of testosterone was 7 months (range 1 to 58). At 3, 6 and 12 months 28%, 48% and 74% of men had normal serum testosterone, respectively. Serum testosterone took significantly longer to return to normal in patients on androgen deprivation therapy for 24 months or greater compared to those on therapy for less than 24 months (log-rank p = 0.0034). There was no statistical significance based on age or type of luteinizing hormone releasing hormone agonist used. CONCLUSIONS: Androgen deprivation has an effect on serum testosterone that extends beyond the cessation of treatment. Serum testosterone should be measured in all men until normalization. These results should be applied to the interpretation of PSA levels after withdrawal of androgen deprivation therapy. In addition, these data have implications regarding dose scheduling and definition of biochemical (PSA) failure after primary therapy.

Adenocarcinoma↗

PubMed2000

Effects of exogenous testosterone on isolated rabbit corpus cavernosum penis.

AIM: To study the effects of exogenous excess of testosterone on the constricting effect of phenylephrine and endothelium-dependent and -independent relaxing effects of different agonists in the corpus cavernosum penis (CCP). METHODS: Specimens of the CCP were obtained from rabbits testosterone for 1 and 2 months and untreated for 2 months after testosterone-treatment for 2 months. Preparations were mounted between two parallel platinum electrodes in organ baths. Responses to phenylephrine, carbachol, and sodium nitroprusside were obtained by adding the reagent cumulatively to the bath. RESULTS: The phenylephrine-induced contractions were decreased with no change in agonist potency (pD2 value) after both 1 and 2 month testosterone-treatment and did not return to control values in corpus cavernosum obtained from rabbits untreated for 2 months after testosterone-treatment for 2 months. Testosterone treatment for 1 or 2 months increased the endothelium-dependent relaxations induced by carbachol and decreased the relaxations elicited by electric stimulation but did not affect the relaxations induced by sodium nitroprusside. These relaxant responses to carbachol and electric stimulation did not return to control values in corpus cavernosum obtained from rabbits untreated for 2 months after testosterone-treatment for 2 months. There were no significant changes in the pD2 values calculated by agonist-induced relaxation responses in all testosterone-treatment groups compared with control group. CONCLUSION: The exogenous excess of testosterone plays an important role in erectile function by a direct action on the relaxant and contractile responses of CCP.

Animals↗

PubMed1975

Gonadotropin-induced proliferation of endoplasmic reticulum in an androgenic tumor and its relation to elevated plasma testosterone levels.

The development of gonadotropin-induced structural change in a testosterone-secreting Leydig cell tumor and its relationship to plasma testosterone levels were studied in castrate, tumor-bearing mice 2 hr after daily injections of human chorionic gonadotropin (HCG). Tumor cells from control animals were small, averaging less than 1.0 X 10(-9) ml in volume, and were poorly differentiated, having very little smooth endoplasmic reticulum (SER) in their cytoplasm. Average plasma testosterone levels in these mice were near 1.3 ng/ml. Although a five-fold rise in plasma testosterone was measured 2 hr after the first HCG injection, no changes in the endoplasmic reticulum were detected at this time. After the second injection, plasma testosterone rose to only twice control levels, while ultra-areas of mixed rough endoplasmic reticulum and SER. Modest amounts of SER had appeared in many tumor cells after the third injection, and plasma testosterone showed a six-fold rise. Between the third and fourth injections, cell volume increased by about 70% as large accumulations of SER appeared in the cytoplasm of most cells. Plasma testosterone again rose to five times control levels. Increased cell volume and abundant SER were maintained by continuing daily injections of HCG, while the 2-hr plasma testosterone response persisted at five to six times the control level. These findings show that a maximal elevation of plasma testosterone can occur prior to changes in the endoplasmic reticulum of Leydig tumor cells. However, they also suggest that daily repetition of the maximal functional response requires that the cells acquire large quantities of newly produced SER.

Animals↗

PubMed2002

Changes in the effect of testosterone on hypothalamic nitric oxide synthetase during sexual maturation. Its relationship with GnRH release.

OBJECTIVES: To determine the effect of testosterone administration to prepubertal (15 days old) and peripubertal rats (30 days old) on hypothalamic nitric oxide synthetase (NOS), and GnRH release. METHODS: Hypothalamic samples containing the anterior preoptic and medial basal areas (APO-MBH) were incubated for 30 minutes in 500 l of Earle's medium with glucose (1 mg/ml) and bacitracin (20 mM). GnRH was determined by RIA in the medium and NOS activity was determined in APO-MBH after 10 min of incubation by the conversion of (14) C arginine to (14) C citrulline. RESULTS: Treatment with testosterone propionate, significantly decreased NOS hypothalamic activity in prepubertal male rats. ( CONTROL: 58.41 +/- 0.85; Testosterone: 25.61 +/- 1.40, p<0.001) and had no effect in peripubertal male rats (CONTROL 49.28 +/- 1.50; Testosterone 51.48 +/- 5.2 pmoles NO/10 min/hypothalamus). On the other hand, in prepubertal rats the treatment decreased Gn-RH release ( CONTROL: 3.62 +/- 0.23; Testosterone: 1.38 +/- 0.11 (pg/ml medium, p<0.001) and had no effect on Gn-RH release in 30 days old rats ( CONTROL: 3.65 +/- 0.33;Testosterone: 4.15 +/- 0.36 pg/ ml, medium). CONCLUSION: These results clearly demonstrated that testosterone has an inhibitory effect on hypothalamic NOS activity in prepubertal rats while it did not affect the concentration of this neurotransmitter system in peripubertal rats. This pattern is similar to that observed with GnRH hypothalamic release since testosterone has an inhibitory effect in prepubertal rats and did not modify the GnRH release in peripubertal rats. Taking into account the well known stimulatory effect of NO on GnRH and the decrease in the sensitivity of GnRH-gonadotrophin axis to the inhibitory feedback effect of testosterone during sexual maturation and the onset of puberty, it is proposed that the changes here described are connected with maturational modifications in the sexual hormones on-GnRH axis connected with the onset of puberty.

Animals↗

PubMedDate not supplied

"Mitochondrial Eve", "Y Chromosome Adam", testosterone, and human evolution.

I suggest primate evolution began as a consequence of increased testosterone in males which increased aggression and sexuality, therefore, reproduction and success. With time, negative effects of excessive testosterone reduced spermatogenesis and started a decline of the group. Approximately 30-40 million years ago, the gene DAZ (Deleted in AZoospermia) appeared on the Y chromosome, increased spermatogenesis, and rescued the early primates from extinction. (Note: DAZ is considered by some to specifically, positively affect spermatogenesis; others suggest it has no effect on spermatogenesis.) Hominid evolution continued with increasing testosterone. The advent of increased testosterone in females of Homo erectus (or Homo ergaster) increased the female-to-male body size ratio, and eventually produced another era of excessive testosterone. Excessive testosterone caused a reduction in population size (bottleneck) that produced the "Mitochondrial Eve" (ME) mechanism. (Only certain females continued during the bottleneck to transmit their mitochondrial DNA.) That is, the ME mechanism culminated, again, in excessive testosterone and reduced spermatogenesis in the hominid line. Approximately 50,000 to 200,000 years ago, a "doubling" of the DAZ gene occurred on the Y chromosome in hominid males which rescued the hominid line with increased spermatogenesis in certain males. This produced the "Y Chromosome Adam" event. The doubling of DAZ allowed further increases in testosterone in hominids that resulted in the increased size and development of the brain. Modern humans periodically fluctuate between the positive and negative consequences of increased levels of testosterone, currently identifiable as the secular trend, increased infections, and reduced spermatogenesis.

Animals↗

PubMed1976

Human chorionic gonadotropin stimulation of Leydig cell function in puberty. Comparison of testosterone response in plasma and urine.

The plasma and urinary testosterone response to one i.m. injection of 5,000 IU human chorionic gonadotropin (HCG) was tested in 45 children and adolescents of several diagnostic entities: testosterone was measured before the injection and on the second, fourth and sixth days thereafter. It was found that there was a better correlation between the testosterone concentrations and the different pubertal stages than between testosterone concentration and either chronological or skeletal age. In the children with normal pubertal development, there was a slight rise in basal testosterone concentration with the progression of the pubertal stages. HCG caused a rise in plasma and urinary testosterone: this response was more marked in pubertal stages 4 and 5. The urinary response was variable whereas the changes in plasma testosterone concentration were more constant. In children and adolescents with primary or secondary hypogonadism, the basal levels of testosterone were low or undetectable and there was only a slight response to the single dose of HCG. It was concluded that a single i.m. injection of 5,000 IU HCG and the determination of plasma testosterone before, and two and four days after injection is a useful screening test for Leydig cell function.

Adolescent↗

PubMedDate not supplied

Evidence that testosterone regulates Leydig cell 3 beta-hydroxysteroid dehydrogenase-isomerase activity by a trans-acting factor distal to the androgen receptor.

Leydig cells are a target for their own steroid product, testosterone, and thus could be subject to short-loop feedback regulation by androgens. The authors previously reported that 3 beta-hydroxysteroid dehydrogenase-isomerase (3 beta HSD) activity was higher in freshly isolated Leydig cells from C57BL/6J than those from C3H/HeJ inbred mice. To determine whether this strain-related difference in 3 beta HSD activity could be mediated by differential sensitivity to feedback effects of testosterone, Leydig cells from the two strains were cultured in the presence or absence of testosterone, the synthetic androgen receptor agonist, mibolerone, or the nonaromatizable androgen, dihydrotestosterone. After 7 days of treatment, all three androgens significantly decreased 3 beta HSD activity in Leydig cells from C57BL/6J, but not from C3H/HeJ mice. When Leydig cells were cultured with hydroxyflutamide, an androgen receptor antagonist, the effect of testosterone was negated. To determine whether the strain-related difference in sensitivity to testosterone was mediated by a difference in the androgen receptor protein, Leydig cells from reciprocal F1 hybrid lines of mice were cultured in the presence or absence of testosterone. Testosterone treatment inhibited 3 beta HSD activity in both F1 lines to the same extent as observed for Leydig cells from C57BL/6J mice. Thus, there is a strain-related difference in the response to testosterone, but it cannot account for the strain-related difference in Leydig cell 3 beta HSD activity because the high 3 beta HSD strain (C57BL/6J) is the sensitive strain. Although the effect on C57BL/6J Leydig cells is androgen receptor-mediated, the dominant effect of testosterone on both F1 lines rules out a difference in the androgen receptor protein per se. However, the data are consistent with the difference being in a trans-acting factor distal to the androgen receptor.

Androgen Receptor Antagonists↗

PubMedDate not supplied

Temporal relationships among testosterone production, steroidogenic acute regulatory protein (StAR), and P450 side-chain cleavage enzyme (P450scc) during Leydig cell aging.

Previous studies have shown that the capacity of Leydig cells from aged (21-24-month-old) Brown Norway rats to produce testosterone is reduced from young (4-month-old) levels, and that this is correlated with reductions in steroidogenic acute regulatory protein (StAR), peripheral benzodiazapine receptor (PBR), and the levels and activities of the steroidogenic enzymes. The age(s) at which particular changes in the steroidogenic pathway occur, and the relationship of particular changes to reduced testosterone production, are not known. We examined 3 critical components of the steroidogenic pathway, cyclic adenosine monophosphate (cAMP) production, StAR, and P450 side-chain cleavage enzyme (P450scc) in relationship to age-related decreases in testosterone production. Leydig cells isolated from Brown Norway rats of increasing ages (4, 9, 15, and 20 months) were evaluated. The ability of Leydig cells to produce testosterone was reduced at 9 months, although not significantly. Significant reductions in testosterone production were first seen in cells isolated from rats of 15 months of age, and further reductions occurred thereafter. Reduced testosterone was correlated with reductions in StAR, P450scc mRNA, and protein. Significant decline in luteinizing hormone-stimulated intracellular cAMP levels was seen by 9 months, before significant reductions in testosterone, StAR, and P450scc. Further declines in cAMP levels were seen at 15 and 20 months. These studies suggest that age-related reductions in intracellular cAMP may lead to the reduced testosterone production that characterizes aged Leydig cells. This suggestion is supported by recent studies from our lab demonstrating that long-term (3 days) culture of old Leydig cells with dbcAMP restored testosterone production to levels approximating those of young cells.

Animals↗

PubMed2005

[Should older men be treated with testosterone?].

BACKGROUND: Male hypogonadism is a clinical situation characterised by a low serum testosterone level in combination with a diversity of symptoms and signs such as reduced libido and vitality, decreased muscle mass, increased fat mass and depression. Similar symptoms in combination with subnormal testosterone levels are seen in some elderly men. Several publications have suggested that testosterone treatment in hypogonadal men may have beneficial effects, but it is still uncertain whether testosterone substitution in the aging man is indicated. Despite this uncertainty the sale of testosterone have increased enormously over the last few years, hence it seems important to discuss what we now know about such treatment. MATERIAL AND METHODS: Review of recent literature studying testosterone substitution in older men. RESULTS AND INTERPRETATION: The result from placebo-controlled studies of testosterone substitution in elderly men differ substantially, but it seems to improve, among other things, bone mineral density, body composition, perception of physical strength, and maybe libido. In the short term there have been few problems or complications with testosterone treatment, but effects on the cardiovascular system and the prostate over the long term remain uncertain. Before any general recommendation could be given, big prospective studies have to be performed. Treatment should, however, be considered in men with testosterone in the hypogonadal range accompanied by clinical symptoms. Treatment needs to be individualized and should preferably be initiated by specialists in andrology, endocrinology or urology.

Age Factors↗