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 1,351 records · Page 75Linked to original sources

PubMed1982

Testosterone inhibition of LRH-induced luteinizing hormone release by cultures of rat anterior pituitary cells: effect of inhibitors of steroid 5 alpha reductase.

Cultures of rat anterior pituitary cells were utilized to examine the role of 5 alpha reduction in the inhibitory action of testosterone on LRH-induced LH release. Cultures were pre-treated with steroids for 48 h and then incubated 6 h with steroids plus 5 x 10(-10) M LRH, the approximate EC50 for LH and FSH release. Testosterone inhibited LRH-induced LH release with an IC50 of approximately 2 x 10(-10) M. However, even relatively high concentrations of testosterone did not completely inhibit LRH-induced release. Testosterone (and dihydrotestosterone) appeared to antagonize LRH-induced LH release but did not markedly affect 48 h basal release or LH synthesis as judged by the quantity of LH released plus that remaining intracellularly. Progesterone (10(-6) M) and heparin (1000 U/ml) were used as inhibitors of anterior pituitary steroid 4 alpha reductase. Progesterone, when combined with testosterone, markedly shifted the testosterone inhibition curve to the right (approximately 340-fold) but did not shift the dihydrotestosterone inhibition curve. Heparin also slightly shifted the testosterone inhibition curve (approximately 2.4-fold) to the right. These observations support the hypothesis that the mechanism of action of testosterone on the anterior pituitary involves 5 alpha reduction.

5-alpha Reductase Inhibitors↗

PubMed1983

Relationship of high density lipoprotein cholesterol with total and free testosterone and sex hormone binding globulin.

A cross-sectional study was performed to see if the previously described association between high density lipoprotein (HDL) cholesterol and plasma total testosterone concentration reflected a relationship with free testosterone or with sex hormone binding globulin (SHBG). In 295 employed middle-aged men, measurements were made of total testosterone and SHBG in serum and of testosterone in saliva, and also of plasma total and HDL cholesterol, plasma triglycerides and other factors which might influence HDL cholesterol levels such as body mass index, alcohol and smoking habits and thyroid hormone levels. In a multiple regression analysis using the GLIM package programme total testosterone concentrations had a persistent positive association with HDL cholesterol (t = 3.5, P less than 0.001) - this association was independent of SHBG (which had a negative association with HDL: t = -1.8, P less than 0.07. The association of HDL cholesterol with testosterone was independent of and stronger than the association of HDL cholesterol with body mass index, alcohol intake and cigarette smoking. Salivary testosterone (a measure of the circulating free hormone) also had a positive independent association with HDL cholesterol. The relationship between HDL cholesterol and testosterone thus appears to reflect an association with circulating hormone levels rather than with the hormone binding globulin.

Alcohol Drinking↗

PubMed1988

Investigations upon the mechanism of inhibition of spermatogenesis in the rat by a dimeric ethynodiol-testosterone ester.

The combination of androgens and progestogens has been shown to be a suitable male contraceptive. Previous experiments revealed that injection of a dimeric testosterone-ethynodiol ester into rats and monkeys induces azoospermia for several weeks. In order to investigate the mechanism of action, we compared the endocrine effects of a single injection of 10 mg of the dimeric ester into intact male rats with that of 6 mg of norethisterone enanthate + 6 mg of testosterone enanthate. After the injection of the dimer there was a transitory reduction of serum FSH and a strong suppression of serum LH and testosterone, of testicular testosterone and of androgen-binding protein (ABP) in the testis and epididymis for at least 8 weeks, whereas spermatogenesis was totally depressed between the 4th and 8th week. Contrary to this, the enanthates caused only a slight suppression of spermatogenesis, although serum LH, testicular testosterone and ABP were profoundly reduced. The only conspicuous difference in the endocrine pattern of both groups during the first 4 weeks was in the serum testosterone level which remained normal in the rats treated with the enanthates. The results suggest that testicular testosterone and ABP concentrations are of minor significance for an intact spermatogenesis, and that some other factors produced by Sertoli cells might be involved and possibly maintained by normal serum testosterone levels.

Androgen-Binding Protein↗

PubMed1988

Substitution therapy of hypogonadal men with transdermal testosterone over one year.

Current testosterone substitution therapy either by injectable or oral testosterone esters suffers from markedly fluctuating serum testosterone levels often far above or below the physiological range. Recently, a transdermal therapeutic system (TTS) for the delivery of testosterone was developed which, when applied to the scrotum, provides smooth serum testosterone levels. Here we report results from seven hypogonadal men treated with the TTS for 14 months by applying a new patch every day. In all patients serum testosterone and dihydrotestosterone (DHT) determined 3-5 h after applying a new patch increased significantly and remained within the physiological range during the entire treatment period. The DHT/testosterone ratio remained constant. In 4 of these patients and 2 others under TTS treatment serum testosterone and DHT were also determined over a 24-h period at regular intervals. In these patients serum testosterone levels in the physiological range were seen during the entire observation period, whereas an increase in the DHT/testosterone ratio occurred towards the end of the one-day treatment phase. All patients in the 14-month treatment study were clinically well substituted and responded with good compliance. Clinical chemistry showed no abnormalities during treatment. Thus, the TTS appears to be an effective and safe new modality for the treatment of male hypogonadism.

Administration, Cutaneous↗

PubMed1989

Testosterone and its binding in hyperthyroid women before and under antithyroid drug therapy.

The serum concentrations of the different forms of circulating testosterone, total testosterone, free testosterone and non-sex-hormone binding globulin bound testosterone (albumin bound + free fractions) which is considered as the bioavailable hormone, were measured in 15 hyperthyroid women before and after anti-thyroid drug therapy and in 15 age-matched healthy women. Sex-hormone binding globulin and albumin were quantified. Total testosterone was significantly higher in hyperthyroid women before treatment, whereas free testosterone and non sex-hormone binding globulin bound testosterone were significantly decreased. After recovery, all the parameters returned to the normal range. In hyperthyroid patients, the variations in the different fractions of testosterone can be related to the rise of sex-hormone binding globulin. These variations could be explained by the displacement of the equilibrium defined by the binding equation.

Adult↗

PubMed1989

5 alpha-reductase activity regulates testosterone accumulation in two bands of immature cultured Leydig cells isolated on Percoll density gradients.

The 5 alpha-reductase inhibitor, 4-methyl-4-aza-3-oxo-5 alpha-pregnan-20(s)-carboxylate was utilized to examine maturational changes in testosterone synthesizing capacity of Leydig cells localizing in Band 2 and Band 3 of Percoll density gradients. Immature Band 2 Leydig cells (from 25- to 39-day-old rats) cultured without the 5 alpha-reductase inhibitor, produced increased testosterone in response to hCG or 8-br-cAMP; however, basal, hCG- or 8-br-cAMP-stimulated testosterone accumulation was 4- to 12-fold higher when cells were cultured in the presence of inhibitor. Band 2 cells from older rats produced much less testosterone in response to hCG or 8-br-cAMP (less than 3.5 pmol/10(5], even when cultured with the inhibitor. Although immature Band 3 cells cultured in the absence of 5 alpha-reductase inhibitor produced increased testosterone in response to hCG or 8-br-cAMP, testosterone levels were relatively low, because elevated 5 alpha-reductase prevented appreciable androgen accumulation; however, Band 3 cells from older rats (over 39 days old) accumulated progressively more testosterone, because of the age-dependent decline in 5 alpha-reductase activity. Immature Band 3 cells cultured with the 5 alpha-reductase inhibitor accumulated 20- to 44-fold more testosterone in response to hCG of 8-br-cAMP.(ABSTRACT TRUNCATED AT 250 WORDS)

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗

PubMed1996

Testosterone-induced increase of insulin-like growth factor I levels depends upon normal levels of growth hormone.

Pubertal development is associated with a rise in plasma insulin-like growth factor I (IGF-I) levels that is related both to the increase in sex steroids and/or to the sex steroid-induced augmentation in endogenous growth hormone (GH) secretion. In order to investigate the relationship between IGF-I, GH and testosterone, we examined 42 male subjects with various clinical conditions (classical GH deficiency (CGHD, N = 5), non-classical GH deficiency (NCGHD, N = 7), short idiopathic stature (N = 6), nutritional obesity (N = 8), GH-treated CGHD (N = 4), GH-treated NCGHD (N = 5) and normal stature (N = 7)) in which , for evaluation of hypogonadism (i.e. the absence of one or both testes from the scrotal sac), human chorionic gonadotropin (hCG) tests were performed. We measured IGF-I, total and free testosterone and dehydroepiandrosterone sulfate (DHEAS) by radioimmunoassays before and 48 and 96 h after the start of the test. The values of IGF-I were lower (0.001 < p < 0.005) in CGHD and NCGHD than in the other groups. In comparison to basal levels, IGF-I values increased (0.005 < p < 0.05) both 48 and 96 h after the start of the hCG test in short idiopathic and normal stature children and in GH-treated subjects with NCGHD, but only 96 h in subjects with untreated NCGHD and GH-treated CGHD. No difference was demonstrated in basal values of total testosterone among any of the groups, while basal free testosterone levels were higher (0.001 < p < 0.05) in GH-treated subjects with NCGHD than in all the other groups except nutritional obesity; furthermore, free testosterone was higher (p < 0.05) in nutritional obesity than in CGHD. The values of total and free testosterone obtained both 48 and 96 h after the start of the hCG test were higher (0.001 < p < 0.05) than basal values in all groups. The DHEAS values did not show any significant change during the hCG test. Basal values were higher (0.01 < p < 0.05) in nutritional obesity than in the other groups. Considering all groups, chronological age, bone age and bone age/chronological age ratio were correlated with basal free testosterone, IGF-I and DHEAS levels (0.001 < p < 0.05), while basal free testosterone and IGF-I values were correlated with DHEAS levels (p < 0.005 and < 0.01, respectively). In conclusion, our study during the hCG test in boys with various clinical conditions demonstrated an increase in IGF-I concentrations only in those boys with sufficient GH secretion or GH replacement therapy. These findings indicate that both sex steroids and GH are necessary to allow for the pubertal increase in IGF-I levels.

Body Height↗

PubMed2002

Testosterone substitution of hypogonadal men prevents the age-dependent increases in body mass index, body fat and leptin seen in healthy ageing men: results of a cross-sectional study.

INTRODUCTION: In healthy men, body weight and total fat content increase with advancing age, while serum testosterone levels decrease. In order to elucidate whether a causal relationship between these phenomena exists, we investigated the influence of testosterone or human chorionic gonadotrophin substitution on body mass index (BMI), total fat mass and serum leptin in testosterone-treated and untreated hypogonadal patients in comparison with ageing eugonadal men. METHODS: In a cross-sectional study, the inter-relationships of body weight, total fat mass, serum sex hormones and leptin were analysed in untreated hypogonadal men (n=24; age 19-65 years), treated hypogonadal men (n=61; age 20-67 years) and healthy eugonadal men (n=60; age 24-78 years). Total fat mass was assessed by bioimpedance measurement. Univariate and multiple linear regression analysis was used to detect possible differences. RESULTS: In eugonadal men, serum testosterone levels decreased with advancing age (correlation coefficients: r=-0.71; P<0.0001), while BMI (r=0.39; P=0.002), total fat content (r=0.51; P<0.0001) and leptin (r=0.48; P<0.0001) increased significantly. In untreated hypogonadal patients, an increase in BMI (r=0.50; P=0.013) and total fat mass (r=0.41; P=0.044) was also observed with advancing age. However, in substituted hypogonadal patients, no age-dependent change in BMI (r=0.067; P=0.606), body fat content (r=-0.083; P=0.522), serum testosterone (r=-0,071; P=0.59) or serum leptin (r=-0.23; P=0.176) was found. CONCLUSION: Since testosterone-substituted older hypogonadal men show BMI and fat mass similar to those of younger eugonadal men and since non-treated hypogonadal men are similar to normal ageing men, testosterone appears to be an important factor contributing to these changes. Thus ageing men should benefit from testosterone substitution as far as body composition is concerned.

Adipose Tissue↗

PubMed2004

A mathematical comparison of techniques to predict biologically available testosterone in a cohort of 1072 men.

OBJECTIVE: In the absence of widely available measures of determining free and/or bioavailable testosterone (BioT) physicians may use formulae such as the free androgen index (FAI) to estimate free testosterone. We compared the efficacy of calculated markers of androgen status in predicting serum BioT and hypogonadism. DESIGN: Total testosterone (TT), sex hormone binding globulin (SHBG) and BioT were determined in a large cohort of men. Comparison of calculated androgen levels was performed following endocrine assessment. METHODS: TT and SHBG were determined by ELISA, and BioT was determined by ammonium sulphate precipitation. From these data we calculated FAI and free testosterone using two other published formulae - FTnw (free testosterone as calculated by the method of Nanjeee and Wheeler) and FTv (free testosterone as calculated by the method of Vermeulen). A novel formula was derived to calculate BioT from given levels of TT and SHBG (BTcalculated). The ability of the methods (FAI, FTnw, FTv, BTcalc) to predict BioT were compared using regression analysis. The ability of these markers of androgen status to predict biochemical hypogonadism was compared using area under receiver operator curve (auROC). RESULTS: The equation derived from our data was the best predictor of BioT (R(2)=0.73, P<0.0001) although TT was also a good marker (R(2)=0.68, P=0.0001). In the determination of hypogonadism, of all currently available formulae none were better that the TT (auROC: TT=0.93, FAI=0.72, FTnw=0.91, FTv=0.88) although when TT is borderline (7.5<TT<12 nmol/l) estimates of free testosterone are superior to TT alone (auROC: TT=0.63, FAI=0.74, FTnw=0.75 and FTv=0.75). CONCLUSIONS: TT is the best marker of hypogonadism and BioT, when TT is borderline calculated indices of free testosterone or BioT are useful and may help confirm hypogonadism.

Biomarkers↗

PubMed2006

Testosterone replacement therapy improves insulin resistance, glycaemic control, visceral adiposity and hypercholesterolaemia in hypogonadal men with type 2 diabetes.

OBJECTIVE: Low levels of testosterone in men have been shown to be associated with type 2 diabetes, visceral adiposity, dyslipidaemia and metabolic syndrome. We investigated the effect of testosterone treatment on insulin resistance and glycaemic control in hypogonadal men with type 2 diabetes. DESIGN: This was a double-blind placebo-controlled crossover study in 24 hypogonadal men (10 treated with insulin) over the age of 30 years with type 2 diabetes. METHODS: Patients were treated with i.m. testosterone 200 mg every 2 weeks or placebo for 3 months in random order, followed by a washout period of 1 month before the alternate treatment phase. The primary outcomes were changes in fasting insulin sensitivity (as measured by homeostatic model index (HOMA) in those not on insulin), fasting blood glucose and glycated haemoglobin. The secondary outcomes were changes in body composition, fasting lipids and blood pressure. Statistical analysis was performed on the delta values, with the treatment effect of placebo compared against the treatment effect of testosterone. RESULTS: Testosterone therapy reduced the HOMA index (-1.73 +/- 0.67, P = 0.02, n = 14), indicating an improved fasting insulin sensitivity. Glycated haemoglobin was also reduced (-0.37 +/- 0.17%, P = 0.03), as was the fasting blood glucose (-1.58 +/- 0.68 mmol/l, P = 0.03). Testosterone treatment resulted in a reduction in visceral adiposity as assessed by waist circumference (-1.63 +/- 0.71 cm, P = 0.03) and waist/hip ratio (-0.03 +/- 0.01, P = 0.01). Total cholesterol decreased with testosterone therapy (-0.4 +/- 0.17 mmol/l, P = 0.03) but no effect on blood pressure was observed. CONCLUSIONS: Testosterone replacement therapy reduces insulin resistance and improves glycaemic control in hypogonadal men with type 2 diabetes. Improvements in glycaemic control, insulin resistance, cholesterol and visceral adiposity together represent an overall reduction in cardiovascular risk.

Abdominal Fat↗

PubMed2006

The androgen receptor CAG repeat modifies the impact of testosterone on insulin resistance in women with polycystic ovary syndrome.

OBJECTIVE: Hyperandrogenism is a central feature of the polycystic ovary syndrome (PCOS) and might worsen insulin resistance (IR) often seen in PCOS. Androgens act through the androgen receptor (AR). A polymorphic CAG repeat sequence within the AR gene was reported to modulate its transactivation activity. Therefore, we investigated a putative interaction between testosterone and the CAG repeat length polymorphism with respect to IR. DESIGN: In 63 PCOS women with normal glucose tolerance free testosterone, the biallelic CAG repeat length and a multiplicative interaction term were investigated by multiple linear regression analysis for an association with IR as indicated by the homeostasis model assessment of IR (HOMA-IR). RESULTS: Free testosterone was correlated with HOMA-IR. The impact of testosterone on HOMA-IR was modified by the AR CAG length as indicated by an interaction term. This interaction remained significant after adjustment for smoking, age and body mass index. While there was a positive association of free testosterone with HOMA-IR, the interaction term was inversely associated. The model, which explained 42.5% of the variation of HOMA-IR predicted that in carriers of short CAG lengths, an increase in testosterone increased IR. This effect attenuated with rising biallelic CAG length until it turns into the opposite at a CAG length longer than 23. The results were confirmed by using CIGMA as another measure of IR. CONCLUSIONS: The association between testosterone and IR is modified by the CAG repeat polymorphism within the AR. Therefore, the evaluation of testosterone effects on IR seems to require consideration of the AR CAG repeat polymorphism in PCOS women.

Adult↗

PubMed2006

Prenatal testosterone and gender-related behaviour.

Testosterone plays an important role in mammalian brain development. In neural regions with appropriate receptors testosterone, or its metabolites, influences patterns of cell death and survival, neural connectivity and neurochemical characterization. Consequently, testosterone exposure during critical periods of early development produces permanent behavioural changes. In humans, affected behaviours include childhood play behaviour, sexual orientation, core gender identity and other characteristics that show sex differences (i.e. differ on average between males and females). These influences have been demonstrated primarily in individuals who experienced marked prenatal hormone abnormalities and associated ambiguities of genital development (e.g. congenital adrenal hyperplasia). However, there is also evidence that testosterone works within the normal range to make some individuals within each sex more sex-typical than others. The size of testosterone-related influences, and perhaps even their existence, varies from one sex-typed characteristic to another. For instance: prenatal exposure to high levels of testosterone has a substantial influence on sex-typical play behaviour, including sex-typed toy preferences, whereas influences on core gender identify and sexual orientation are less dramatic. In addition: there appears to be little or no influence of prenatal testosterone on mental rotations ability, although mental rotations ability shows a marked sex difference. These findings have implications for basic understanding of the role of testosterone in normative gender development, as well as for the clinical management of individuals with disorders of sex development (formerly called intersex syndromes).

Adrenal Hyperplasia, Congenital↗

PubMed1986

Regional differences in the testosterone to dihydrotestosterone ratio in the epididymis and vas deferens of adult mice.

The concentrations of testosterone and dihydrotestosterone (DHT) were measured in the testis and in different segments of the epididymis and vas deferens of adult mice. There were marked regional variations in the concentrations of testosterone and DHT from the testis to the caudal part of the vas deferens. In the testis, testosterone was the predominant androgen (364 +/- 90 ng/g) while DHT was weakly represented (8 +/- 2 ng/g). Qualitative and quantitative changes occurred in epididymis: DHT was the main steroid in the caput (29.3 +/- 2.7 ng/g) and corpus (33.1 +/- 4.4 ng/g) while testosterone and DHT were in similar quantities in the cauda (18.6 +/- 2.6 and 19.0 +/- 2.7 ng/g, respectively). The proximal region of the vas deferens contained higher amounts (71.4 +/- 8.0 ng/g) of androgens (testosterone + DHT) than did the caput epididymidis (39.1 +/- 3.3 ng/g). Testosterone was the predominant androgen in each part of the vas deferens and its concentrations decreased from the proximal (64.5 +/- 7.5 ng/g) to the caudal (26.9 +/- 4.3 ng/g) region. Castration and section of the efferent ducts of the testis showed that the epididymis received testosterone essentially via the blood supply and that epididymal DHT was produced locally from circulating testosterone.

Animals↗

PubMed1989

Effect of testosterone on serum immunoactive inhibin concentrations in intact and hypophysectomized male rats.

Intact and hypophysectomized rats were treated with graded doses of testosterone via subcutaneous Silastic implants over a 13-week period. Serum inhibin concentrations fell 50% (P less than 0.001) after 2 weeks of hypophysectomy, remaining suppressed at this level for 13 weeks. The administration of testosterone to hypophysectomized rats (serum testosterone values 2-12 ng/ml; control values 5.5 ng/ml) was without effect on serum inhibin values. In contrast, administration of testosterone to intact animals for 7 weeks resulted in an initial fall (P less than 0.05) in inhibin levels to 50-70% of controls then increasing to reach control levels at higher doses. Serum FSH concentrations were similarly biphasic with increasing dose of testosterone and values for these two hormones were significantly correlated (r = 0.44, P less than 0.01). Segments of seminiferous tubules in culture from rats after various times of hypophysectomy showed a partly suppressed secretion of inhibin. The administration of testosterone did not modify inhibin production although inhibin production was sensitive to FSH. It is concluded that (1) serum inhibin concentrations are partly suppressed after hypophysectomy and testosterone has no effect on serum inhibin values; and (2) the suppression of serum inhibin in intact rats treated with increasing doses of testosterone is attributable to the concomitant fall in serum FSH concentrations.

Animals↗

PubMed1991

Testosterone and corticosterone co-regulate messenger RNA coding for secretory proteins in the epididymis of the lizard (Lacerta vivipara).

The hormonal requirements for the regulation of Lv132 mRNA coding for two proteins secreted by the principal cells of the lizard epididymis were examined by organotypic culture experiments. Testosterone, R1881 and corticosterone induced accumulation of Lv132 mRNA in explants from lizards castrated immediately after differentiation of the principal cells. The induction by testosterone was inhibited by the addition of cyproterone acetate. Progesterone and oestradiol alone or in presence of testosterone were ineffective. Unlike the induction by testosterone, the effect of corticosterone did not require binding on the androgen receptor as shown by competition binding studies. Corticosterone failed to induce gene expression in organs containing only reserve cells in their epithelium at the onset of the culture. However, corticosterone plus testosterone had a synergistic effect. These data suggest that testosterone promotes the differentiation of principal cells from reserve cells during the culture time and that a primary action of testosterone is necessary to confer corticosterone responsiveness on this tissue. Furthermore, the primary effects of testosterone could be memorized by the tissue because the corticosterone responsiveness persists after castration.

Animals↗

PubMed1993

[Effects of repeated restraint stress at 30-minute intervals during 24-hour on serum testosterone, LH and glucocorticoids levels in male Japanese monkeys (Macaca fuscata)].

We investigated effects of frequent blood collections under the compulsory restraints on serum testosterone, LH and glucocorticoids in adult male Japanese monkeys. Blood samples were withdrawn from three animals at 30-min intervals and two animals at 4-hr intervals during 24 hr. Serum testosterone and LH were measured by a radioimmunoassay, and glucocorticoids was determined by a competitive protein binding assay. Sampling at 4-hr intervals during 24 hr revealed diurnal changes in serum testosterone and glucocorticoids. Levels of testosterone were high throughout the night and low at the day time, conversely serum glucocorticoids were high levels in the morning and low in the evening. On the other hand, 30-min intervals sampling, serum testosterone levels decreased and glucocorticoids levels increased, respectively, immediately after the start of blood sampling. And then, low in testosterone and high in glucocorticoids levels were continually maintained. But serum LH levels had the pulsatile pattern and did not change markedly during 24 hr. After ACTH administration in five animals, serum glucocorticoids levels increased markedly and also testosterone levels increased slightly, but LH levels did not change. These data indicated that the every 30-min restraint stress caused the increment of glucocorticoids levels and the suppression of testosterone levels, but did not affect the serum LH levels. The increased glucocorticoids might inhibit the testicular steroidogenesis, without suppressing the LH secretion from the pituitary.

Animals↗

PubMed2004

The effects of FSH and of testosterone on the completion of meiosis and the very early steps of spermiogenesis of the rat: an in vitro study.

The role of FSH and of testosterone in spermatogenesis has been a matter of controversy. In the present study, we addressed the involvement of these hormones in the regulation of the completion of meiosis of male rats under in vitro conditions. In the first series of experiments, middle/late pachytene spermatocytes were cocultured with Sertoli cells for 2 weeks in the absence or presence of FSH and/or testosterone. Treatment with both FSH and testosterone reduced slightly the percentage of apoptotic germinal cells in the cultures. Moreover, the number of round spermatids formed in vitro was enhanced by FSH or testosterone when compared with control cultures. Neither hormone influenced the half-life of round spermatids under the present culture conditions. The amounts of TP1 mRNAs in FSH- or FSH plus testosterone-treated cultures were higher than those of controls. In another series of experiments, round spermatids were incubated for 24 h in media conditioned by Sertoli cells cultured in the absence or presence of FSH and/or testosterone. TP1 mRNA contents of round spermatids incubated in media from Sertoli cells cultured in the presence of FSH and/or testosterone were two- to threefold higher than those of spermatids incubated in media from Sertoli cells cultured without hormones. These results indicate that FSH and testosterone have positive and somewhat overlapping effects on the meiotic divisions and the post-meiotic expression of a germ cell-specific gene, effects which cannot be related solely to their ability to reduce germinal cell apoptosis. Use of this culture system should help to test the effect of any hormone or factor on those steps in order to understand better their regulation.

Animals↗

PubMed1976

Testosterone concentration in the fluids of seminiferous tubules, the interstitium and the rete testis of the rat.

Testosterone was measured by radioimmunoassay in interstitial fluid, 'free-flow' seminiferous tubular fluid, obtained by micropuncture, and rete testis fluid from intact adult anaesthetized rats. Under non-stimulated conditions the concentration of testosterone in interstitial fluid was below the limit of detection in two rats and achieved a mean level of 150 +/- 27 (S.E.M.) ng/ml in the remaining 17 determinations. The testosterone concentration of the seminiferous tubular fluid was below the limit of detection in two rats, and had a mean level in the remaining 15 determinations of 91 +/- 14 ng/ml, which is significantly lower (P less than 0-02) than that in interstitial fluid. The mean ratio of seminiferous tubular:interstitial fluid testosterone concentration calculated in 14 rats was 0-94 +/- 0.24. This ratio was less than unity whenever the interstitial fluid testosterone concentration was more than 50 ng/ml, whereas in all animals with interstitial fluid testosterone of 50 ng/ml, or less, the ratio was greater than or equal to one. The mean testosterone concentration of rete testis fluid in 32 samples was 33 +/- 3 ng/ml. After HCG stimulation in 12 rats, testosterone concentration in interstitial fluid increased to a mean value of 660 +/- 83 ng/ml, and in seminiferous tubular fluid to 460 +/- 44 ng/ml; the difference between the two was significant (P less than 0-05). These results are discussed in relation to the presumed dilution of seminiferous tubular fluid in rete testis fluid and the role of androgen-binding proteins in the transport of steroids.

Animals↗