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PubMed1983

Oestrogen secretion by in-vitro perfused testes: species comparison and factors affecting short-term secretion.

Testes from mature rats, rabbits, hamsters, guinea-pigs and dogs were perfused in vitro with added gonadotrophins to study the qualitative and quantitative aspects of oestrogen secretion by these species. After separation by high performance liquid chromatography (HPLC), the major oestrogen secreted by the testes of all five species was oestradiol-17 beta; lesser amounts of oestrone were also detected for all species. Secretion rates of oestradiol and testosterone were determined for one testis from each of six animals of each species after purification by HPLC. Oestradiol and testosterone secretion varied (P less than 0.05) among species on both per testis and per gram of testis bases. The rabbit, which was a high secretor of oestradiol, was used in subsequent experiments to study the factors which affect short-term oestradiol secretion by perfused testes. Luteinizing hormone (NIAMDD-LH-S21) at 100 ng/ml significantly stimulated oestradiol secretion by 2.9-fold and increased testosterone secretion by 155-fold. Follicle-stimulating hormone (NIH-FSH-S11) had no significant effect on secretion of either steroid. In a time-course study in which LH stimulation was started after 45 min of control perfusion, the rates of increase in oestradiol and testosterone secretion over time were similar. Increasing amounts of testosterone added directly to the arterial perfusion medium (0-10 micrograms/ml) resulted in an increase in oestradiol secretion in the absence of gonadotrophins. Oestradiol secretion increased in a dose-dependent manner up to 1.0 microgram testosterone/ml; there was no further stimulation of oestradiol secretion at 10 micrograms testosterone/ml. When testes were perfused with saturating concentrations of testosterone (10 micrograms/ml) neither LH nor FSH at 100 ng/ml increased oestradiol secretion above control values. It appears that the major factor affecting oestradiol secretion by in-vitro perfused rabbit testes is the amount of substrate (testosterone) available for aromatization.

Animals↗
PubMed1998

Intratesticular serotonin affects steroidogenesis in the rat testis.

The effect of intratesticular administration of serotonin (5-HT), ketanserin (5-HT2 receptor antagonist), and 5,7-dihydroxytryptamine (5,7-DHT) (the neurotoxin that destroys serotoninergic neural elements) on steroidogenesis was studied in immature and adult rats. In adults, bilateral intratesticular injection of 5-HT resulted in a significant decrease in basal but not in hCG-stimulated testosterone secretion and in serum testosterone concentration, whereas ketanserin induced a significant rise in steroidogenesis 1 h post-treatment. There was no effect 1 day after administration of 5-HT or ketanserin, and 7 days after the injection of 5,7-DHT. In immature rats 1 day after bilateral testicular administration of ketanserin, basal testosterone secretion in vitro was significantly suppressed. In immature hemicastrates, local injection of 5-HT resulted (1 day post-treatment) in a significant rise in steroidogenesis while administration of 5,7-DHT decreased testosterone secretion 7 days after the injection of the neurotoxin. The results indicate that in adult rats 5-HT exerts a suppressive, whereas in immature rats, a stimulatory action on steroidogenesis occurs. Data also suggest that, in both age groups, the effect of 5-HT is mediated through 5-HT2 receptors. The observation that in immatures administration of the neurotoxin resulted in an effect similar to that found following the treatment with the receptor antagonist suggests that, in this age group, 5-HT derived from local neural elements might also be involved in the control of 5-HT on Leydig cell steroidogenesis.

5,7-Dihydroxytryptamine↗
PubMed2006

Assessment of reproductive status in male echidnas.

This study reports the development and application of techniques to assess the reproductive status of male echidnas. The pattern of testosterone secretion over a 24-h period in five echidnas was documented. Testosterone secretion after injection i.m. of either 1000 IU hCG (n=4) or 4 microg GnRH agonist (n=6) was determined to establish whether this could be used as a practical index of the prevailing steroidogenic capacity of the testes. hCG (1000 IU) was also used to assess seasonal changes in testosterone secretion in six echidnas over a 13-month period. Seasonal changes in testicular volume were examined by transabdominal ultrasonography. Electroejaculation was attempted to monitor seasonal changes in sperm production, which was also determined by spermatorrhea. There was no apparent diurnal pattern of testosterone secretion in echidnas and circulating concentrations of testosterone remained relatively low (maximum 1.2 ng/mL) and stable over 24h. Injection of hCG resulted in an increase (P<0.01; n=4) in testosterone concentration with a peak (2.9+/-0.3 ng/mL) approximately 4h after injection. GnRH also induced an increase (P<0.01; n=6) in circulating testosterone that was apparent after 1h (2.6+/-0.3 ng/mL) and concentrations remained elevated (3.4+/-0.3 ng/mL) for up to 8h after injection. Seasonal changes in testosterone secretion determined after injection of hCG, increased (P=0.03; n=6) from late-autumn, peaked in late-winter, and decreased by early-spring. Testicular volume followed a similar seasonal pattern (P<0.01; n=6) with an increase from late-autumn, peak in winter and a decline in mid-spring. There was no seasonal change in live weight. Electroejaculation was attempted throughout two breeding seasons but no semen was obtained. Spermatorrhoea in the echidna was described for the first time and was subsequently used to assess seasonal sperm production. Spermatozoa were found in the urine from June to September. This study has demonstrated that exogenous hormones can be used to obtain an index of the prevailing steroidogenic capacity of the testes in echidnas, which is not apparent with repetitive non-stimulated samples over 24 h. The assessment of testosterone secretion after injection of trophic hormones provides a valuable and practical procedure for the assessment of reproductive status. Testicular ultrasonography and spermatorrhea are useful in assessing reproductive status and in this study were successfully used to determine seasonal reproduction in captive echidnas.

Animals↗
PubMed1993

Virilizing adrenocortical tumors in adult women. Report of 10 patients, 2 of whom each had a tumor secreting only testosterone.

BACKGROUND: Virilizing adrenocortical tumors are uncommon in adult women. These lesions generally secrete dehydroepiandrosterone (DHEA) and dehydroepiandrosterone sulfate (DHEAS), but not testosterone, which usually is produced by ovarian tumors. Exceptionally, adrenal growths may give off testosterone and no other assessable androgen. The detection of the site of excess testosterone yield is paramount for proper surgery. The true nature of the growth often is unpredictable, even at the time the pathologist examines the surgical specimen. METHODS: The workup in a virilized adult woman relies on biochemical tests such as 24-hour urinary 17-KS and 17-OHCS levels and plasma corticosteroid levels (testosterone, DHEA, DHEAS, and androstenedione), and on modern imaging studies such as ultrasonography, computed tomography, and digital angiography. RESULTS: Among a series of 190 adrenal tumors collected in the last 30-year period, only 10 virilizing growths (5.3%) were detected. Two cases of virilization mixed with cushingoid features were observed. In two other cases, reported in detail, the tumor secreted testosterone only, without other assessable androgens. Seven of the 10 tumors were malignant. CONCLUSIONS: In cases of tumors secreting testosterone only, high-resolution imaging has contributed significantly in pinpointing the site of the growth, whereas dynamic hormone testing, using selective stimulation or suppression studies, has been misleading. The malignant nature of the growth may be revealed only by the presence of metastases, because pleomorphism and capsular and vascular invasion have been detected histologically in clinically benign tumors. The prognosis for large tumors usually is dismal.

Adrenal Gland Neoplasms↗
PubMed1997

Effects of sex hormones on fluid and solute transport in Madin-Darby canine kidney cells.

Polycystic kidney disease progresses more rapidly in men than in women. To investigate the basis for this sexual dimorphism, we exposed Madin-Darby canine kidney (MDCK) cells grown on collagen-coated cell culture inserts to control media, or to estradiol or testosterone (1 nM-1 microM). Compared to control and estradiol-treated cells, testosterone stimulated fluid secretion in a dose-dependent manner, enhancing fluid secretion 4.8-fold at 1 nM and 19.7-fold at 1 microM (0.59 +/- 0.18 vs. 0.03 +/- 0.01 microliter/cm2/hr, P < 0.001). Chloride transport paralleled fluid secretion. Testosterone increased cellular cyclic AMP levels 3.2-fold at 1 nM and 12.3-fold at 1 microM (81.3 +/- 30.7 vs. 6.6 +/- 3.3 pmol/mg protein, P < 0.001). GDP beta S (500 microM), an inhibitor of Gs, and 2',3'-dideoxyadenosine (10 microM), an inhibitor of the catalytic subunit of adenylate cyclase, suppressed testosterone-induced fluid and solute secretion. Neither testosterone nor estradiol had any effect on microsomal Na,K-ATPase activity, cellular proliferation or cellular total protein content. Our studies show that testosterone stimulates fluid secretion and solute transport by MDCK cells by increasing cAMP generation. In vivo, testosterone may contribute to cyst expansion by enhancing fluid secretion. This observation may help explain the worse prognosis of polycystic kidney disease observed in men.

Animals↗
PubMed1997

Interactions between alcohol- and opioid-induced suppression of rat testicular steroidogenesis in vivo.

To examine interactions between alcohol and endogenous opioids in their suppressive effects on rat testicular function, the opioid antagonist naltrexone or the opioid agonist morphine was administered to adult male rats alone or in combination with alcohol. Serum testosterone, testicular interstitial fluid (TIF) testosterone, and TIF volumes were measured to assess testicular function. Naltrexone induced dose-dependent increases in serum and TIF testosterone levels without changes in TIF volume. Alcohol (0.5 g/kg) inhibited naltrexone-induced stimulation of testosterone secretion and shifted the naltrexone dose-response curve to the right. Conversely, naltrexone (0.05 mg/kg) inhibited alcohol-induced suppression of testosterone secretion and shifted the alcohol dose-response curve to the right. Relatively high doses of naltrexone (5 to 30 mg/kg) were needed to stimulate testosterone secretion maximally in rats treated with a low dose of alcohol (0.5 g/kg) and to stimulate normal levels of testosterone secretion in rats treated with a high dose of alcohol (2 g/kg). In addition, combined treatment with 1 and 30 mg/kg of naltrexone and 0.5 to 2 g/kg of alcohol did not alter blood alcohol concentrations significantly, suggesting that the interactions between alcohol and naltrexone were unrelated to gross changes in alcohol metabolism or bioavailability factors. Simultaneous treatments with a low dose of alcohol (0.3 g/kg), near the threshold of efficacy, and low-moderate doses of morphine (0.3 to 3 mg/kg) were not additive in suppressing testosterone secretion, compared with either agent alone. These results support the hypothesis that opioid antagonists can reverse the suppressive effect of alcohol on testicular steroidogenesis, but the results also suggest that endogenous opioids do not exclusively mediate alcohol's effects on testosterone secretion.

Alcoholism↗
PubMed1996

Effects of nitric oxide-related agents on opioid regulation of rat testicular steroidogenesis.

These studies examined whether nitric oxide (NO) mediates opioid suppression of testicular steroidogenesis. Adult male rats were treated with various combinations of a NO synthase (NOS) inhibitor (NG-nitro-L-arginine methyl ester; NAME), a NO donor (isosorbide dinitrate; ISDN), an opioid agonist (morphine, and an opioid antagonist (naltrexone). Serum LH and testosterone and testicular interstitial fluid (TIF) testosterone concentrations were then measured. Inhibition of NO production by NAME reversed morphine-suppressed testosterone secretion; treatment with the NO donor, ISDN, reversed naltrexone-stimulated testosterone secretion. NAME did not alter morphine's effects on LH secretion and attenuated morphine's suppression of hCG-stimulated testosterone secretion, indicating that these effects occur directly in the testes and are not dependent on LH secretion. Even though these effects suggested possible interactions between NO and opioid systems, no additive or synergistic effects were found with suppressive combinations of morphine and ISDN, or with stimulatory combinations of naltrexone and NAME at does that had little effect on testosterone secretion when given alone. These results indicate that opioid and NO exert independent effects on testicular steroidogenesis through separate pathways or mechanisms and that NO does not mediate opioid-induced testicular suppression.

Animals↗
PubMed1993

Ontogenesis of estrogen secretion by porcine fetal testes.

High levels of estrogen secretion is a characteristic of steroidogenesis in the pig testis in both the adult and newborn male. We have now examined the ability of fetal gonads to secrete estrogens, and compared it with testosterone secretion during prenatal development. Fetuses were recovered from sows (N = 33) at 27-114 (term) days of gestation. Gonads were removed for organ culture in TC-199 medium, or used as minced tissues or free cell preparations when taken later in development. Organ cultures were maintained for 96 h with luteinizing hormone added for the last 72 h for one gonad of each pair. Estrone, estradiol-17 beta and testosterone were measured by radioimmunoassay in media samples. Trace amounts of estrone were detected almost as early as testosterone secretion commenced, but quantities sufficient for confirmation by radioimmunoassay after chromatography were not seen until day 35 of gestation. Estrogen production increased to > 0.37 nmol.gonad-1.4 h-1 at term. Testosterone secretion in organ culture was increased by luteinizing hormone but no effect was seen on estrone levels for the first half of pregnancy. Thus, estrogen secretion is a feature of steroidogenesis in the porcine testes even in the early stages of fetal development.

Animals↗
PubMed2000

Effect of intratesticular administration of TRH or anti-TRH antiserum on function of rat testis.

The effect of intratesticular administration of thyrotropin-releasing hormone (TRH) and anti-TRH antiserum on steroidogenesis was studied in immature and adult rats. In 9-day-old animals local administration of the neuropeptide resulted in an increase in basal testosterone secretion in vitro. Similar treatment of 15-day-old rats suppressed hCG-stimulated testosterone secretion with no change in basal testosterone production. In both immature groups the treatment did not affect serum testosterone concentration. By contrast, in adults TRH decreased serum testosterone level, but did not influence basal and hCG-stimulated testosterone secretion. Both in immature and adult rats, the changes in steroidogenesis were evident 1 hour posttreatment. Five days after the administration of anti-TRH antiserum into the remaining testis of immature rats subjected to hemicastration just prior to the antiserum treatment, the alterations in steroidogenesis were opposite to those detected after treatment with TRH. In 9-day-old rats the antiserum suppressed steroidogenesis, while in 15-day-old animals it stimulated testosterone secretion. The results suggest that testicular TRH might exert a local action on testicular steroidogenesis, and the effect is age-dependent.

Aging↗
PubMed1985

Secretion of anti-Müllerian hormone by immature bovine Sertoli cells in primary culture, studied by a competition-type radioimmunoassay: lack of modulation by either FSH or testosterone.

Secretion of anti-Müllerian hormone (AMH) by immature bovine Sertoli cells in primary culture was studied through a competition-type RIA employing a polyclonal antibody and 125I-labelled purified AMH. This RIA is approximately 10 times more sensitive than the solid-phase two-site monoclonal antibody-based RIA described previously. Biosynthesis and secretion of AMH by cultured Sertoli cells require approximately 48 h, are not influenced by FSH or testosterone and steadily decrease over a one-week period of culture. Cyclic AMP response to FSH stimulation is normal in cultured cells. Whether the factors responsible for the extinction of AMH production in vitro are in any way related to those operating during normal maturation, which lead to repression of AMH biosynthesis in adult Sertoli cells, is not known at the present time and deserves further study.

Age Factors↗
PubMed1989

Adrenalectomy does not influence basal secretion of testosterone in rat in vivo.

We have studied the effect of adrenalectomy on the testicular secretion of testosterone in the rat. In the acute period following adrenalectomy plasma testosterone levels were reduced but this was no different from those levels in appropriate sham-operated controls. This reduction in plasma testosterone levels is probably a result of direct effects of anaesthesia and surgical stress. Whilst studies on the late effect of adrenalectomy avoided this problem, plasma testosterone levels were normal in both adrenalectomised and sham-operated animals. Resetting of anterior pituitary-gonadal relationships may mask the absence of any contribution made by the adrenal gland to testicular steroidogenesis. In contrast to previous data we were unable to demonstrate that adrenalectomy influenced the secretion of testosterone in the male rat.

Adrenalectomy↗
PubMed1994

The "female effect" in Australian cashmere goats: effect of season and quality of diet on the LH and testosterone response of bucks to oestrous does.

The effects of season, diet and exposure to oestrous females on LH and testosterone secretion were examined in mature cashmere bucks to determine whether there is a seasonal cycle of LH and testosterone secretion, and whether this can be modulated by long-term differential nutrition and exposure to oestrous females. Three-year-old bucks were individually housed under natural photoperiod at 29 degrees S 153 degrees E and fed diets of high (crude protein 17.6%, metabolizable energy 8.3 MJ kg-1) or low (crude protein 6.9%, metabolizable energy 6.6% MJ kg-1) quality for 16 months ad libitum (n = 6 per treatment). Blood samples were collected to determine pulsatile LH and testosterone secretion immediately before experimental feeding, one month later, and every second month thereafter. Samples were collected for an 8 h period on successive days with the bucks isolated on the first day and each exposed to a single oestrous doe for the duration of the second day. In the absence of oestrous females, bucks exhibited a circannual pattern of secretion for both hormones with pulse frequency and mean concentrations highest in late summer and autumn and lowest in late winter and spring. Testosterone pulse amplitude followed a similar pattern, but LH pulse amplitude was highest in spring and lowest in autumn, indicating a seasonal shift in the relationship between the two hormones. Exposure to oestrous does increased LH and testosterone secretion depending on both season and diet. Responses were evident during summer, autumn and early winter, with bucks on a high quality diet exhibiting an earlier and more prolonged period of responsiveness than did bucks on a low quality diet, peaking in February compared with June. The magnitude of the LH and testosterone response was also significantly greater in bucks on a high quality diet. Weight loss during autumn appeared to reduce responsiveness in both treatments. These results demonstrate that there is a seasonal cycle in LH and testosterone secretion in mature cashmere bucks, and that nutrition and oestrous females are powerful modulators of the secretion of these hormones in a seasonally dependent way.

Animals↗
PubMed1993

Opioid-induced suppression of rat testicular function.

The effects of opioids on testicular function were assessed in the rat through measurements of serum testosterone levels, testicular interstitial fluid (TIF) formation and TIF testosterone levels after morphine and opioid antagonist (naloxone, naltrexone) treatment. Serum and TIF levels of testosterone were significantly decreased 1 to 6 h after morphine (10 mg/kg) injection, and TIF volumes were decreased 2-3 h after injection morphine. Each of these decreases was dose-related. In contrast to the effects of morphine, the opioid antagonist naloxone increased TIF testosterone but did not alter TIF volumes. Moreover, the opioid antagonist naltrexone totally blocked morphine's effects on both testosterone secretion and TIF volume, suggesting that morphine's testicular effects were mediated by naltrexone-sensitive opioid receptors in the testes. The possible role of morphine-induced reductions in gonadotropin secretion in morphine's testicular effects was also examined. Morphine suppressed testosterone secretion and TIF volumes after pretreatment with human chorionic gonadotropin, which reverses morphine's suppression of luteinizing hormone (LH). Our results, therefore, indicate that morphine exerts effects on testicular function that are independent of its effects on LH. They furthermore support the hypothesis that both endogenous and exogenous opioids disrupt two major aspects of testicular function: Testosterone secretion and TIF formation. Because of the role of TIF in maintaining testicular function, our results suggest that opioid-induced changes in testosterone secretion into TIF and TIF formation may, at least in part, explain the well-established effects of opioids on reproductive endocrinology and function in the male.

Animals↗
PubMed1979

Effect of treatment with an agonist of luteinizing hormone releasing hormone on early maturational changes in pituitary and testicular function in the rat.

Male rats aged 30 days were injected once daily for between 1 and 7 days with 50 ng (D-serine t-butyl6, des-glycine-NH210) luteinizing hormone releasing hormone ethylamide (LH-RH agonist), and pituitary and testicular function were assessed. Treatment for 7 days significantly (P less than 0.02) inhibited maturational increases in the pituitary content and serum concentration of gonadotrophins, testicular luteinizing hormone (LH)-receptor concentration and the testicular capacity to secrete testosterone; the pituitary content and serum concentration of prolactin, the hypothalamic content of LH-RH and testicular weight were unaffected. In rats treated with LH-RH agonist, the initial (2 to 3 days) reduction in testicular LH-receptors and the capacity to secrete testosterone probably resulted from acutely raised levels of LH in the blood, whilst later effects may have resulted from the apparently chronic reduction in serum gonadotrophin levels. The latter may reflect a decrease in pituitary responsiveness to repeated stimulation with LH-RH agonist. Despite the extensive loss of testicular LH-receptors and diminished responsiveness, the concentration of HCG which significantly (P less than 0.05) increased testosterone secretion by the testis in vitro was the same (2 pmol/l) as that for testes from control rats.

Animals↗
PubMed1996

Splenic macrophages can modify steroidogenesis of Leydig cells.

A large amount of LH/hCG treatment given to male rats is known to suppress the enzyme activity of cytochrome P450c17 in Leydig cells for 48 h. A high dose LH/hCG injection is also known to allow immunocytes, such as macrophages, to migrate into the testicular interstitial compartment. It has not been known, however, whether these cells play a role in that suppression. In this study, we examined if splenic macrophages have any effects on testosterone secretion from Leydig cells by culturing rat testicular interstitial cells (TIC). Splenic macrophages co-cultured with TIC significantly suppressed testosterone secretion. Macrophages co-cultured reduced both progesterone to testosterone conversion and the amount of cytochrome P450c17 mRNA. The conditioned medium (SMCM), prepared by culturing macrophages for 12 h, significantly reduced either testosterone secretion from TIC or progesterone to testosterone conversion by TIC. These results indicate that splenic macrophages suppress testosterone secretion from Leydig cells by suppressing the cytochrome P450c17 enzyme in vitro, and that this effect is mediated at least in part by some soluble factors secreted from macrophages. Splenic macrophages migrating into the testis after LH/hCG stimulation could play a role in suppressing cytochrome P450c17 in Leydig cells.

Animals↗
PubMed1976

Testicular response to exogenous gonadotropins in the syndrome of feminizing testes.

The steroid response of testes to exogenous gonadotropin administration was studied before castration in a patient with the complete form of the testicular feminization syndrome. Urinary steroid determination were made along with measurements of plasma testosterone during adrenal suppression with dexamethasone and after stimulation with human menopausal gonadotropin (HMG) and HMG plus human chorionic gonadotropin (HCG). Our data provide evidence that the gonads in the testicular feminization syndrome synthesize steroids normally. Estrogens and testosterone are secreted by the testes, and the Leydig cells of the testes are capable of responding to exogenous HMG and HCG stimulation. These findins are consistent with the hypothesis that there is no abnormal testicular steroidogenesis in these genotypic males. Additional evidence is provided that these gonads secrete testosterone in amounts comparable to those of normally functioning testes. Failure of virilization in the presence of androgen secretion as indicated by previous authors is probably the result of a deficiency of androgenic action at the end organs. The presence of sparse pubic and axillary hair in the mother and the finding of the same type of karyotype (46,XY) in a sibling suggest that hereditary factors play a role in this disorder.

17-Ketosteroids↗
PubMed1993

The effect of diabetes on sexual behavior and reproductive tract function in male rats.

The effect of streptozotocin induced diabetes and sabeluzole (SBZ) on sexual function was evaluated in male rats. SBZ is a benzothiazole derivative with antihypoxic and antiischaemic activities. Rats were rendered diabetic by intraperitoneal injection of streptozotocin, 60 mg./kg. body weight, and either left untreated or treated with 1.0 mg./kg. of SBZ. Two groups of control rats treated with or without SBZ were also evaluated. Seven weeks after the induction of diabetes, all rats were studied in vivo for mating behavior. Animals were sacrificed one week later, and detrusor strip response in vitro was evaluated. The reproductive organ weight, sperm content and motility as well as in vitro testosterone secretion and serum levels of LH and testosterone were determined. Diabetes induced significant reduction in mating behavior. The diabetic rats that received SBZ showed a significant improvement in mating behavior. The percentage of animals that exhibited ejaculation was 0% in the diabetic group compared to 70% in the controls and 38% in diabetic plus SBZ group. The strips of the detrusor muscle of the diabetic group showed a marked hypersensitivity to bethanechol HCL. In the diabetic plus SBZ group, the strips of the detrusor muscle showed a response similar to that of the control. The diabetic rats had significantly diminished reproductive organ weight, testicular sperm content, epididymal sperm content and sperm motility relative to the control. In addition, marked decrease in the serum level of testosterone and in vitro testosterone secretion was observed in diabetic rats. In the diabetic plus SBZ group, the reproductive organ weight, sperm content and motility as well as serum testosterone and in vitro testosterone secretion showed an improvement compared to diabetic rats. In summary, our data suggest that sex behavior and reproductive tract functions are markedly affected by streptozotocin induced diabetes. Sabeluzole treatment could be beneficial in reducing the deleterious effect of diabetes on sexual functions.

Animals↗
PubMed1993

Spontaneous gonadotropin and testosterone concentration profiles in prepubertal and pubertal boys: temporal relationship between luteinizing hormone and testosterone.

To investigate the detailed pattern of change in circulating gonadotropin and testosterone concentrations around the onset of puberty and to determine the temporal relationship between the gonadotropin and testosterone secretion, plasma gonadotropin and testosterone were measured at 20-min intervals for 24 h in 21 normal short boys. The obtained plasma hormone concentrations were analyzed by Cluster pulse detection algorithm, cosinor analysis, and cross-correlation analysis. The 21 subjects were divided into the prepubertal (n = 16) and early pubertal (n = 5) groups. All subjects showed nocturnal LH and FSH pulses and had significant circadian LH and FSH rhythms. Except for six boys of prepubertal group, all subjects showed nocturnal testosterone pulses and had significant circadian testosterone rhythms. The acrophase (clocktime of maximal value) of circadian testosterone rhythm was 0308-0428 h. Cross-correlation analysis demonstrated significant positive cross-correlations between LH and testosterone that were maximum at a testosterone lag of 60-120 min. Further, to eliminate intrinsic autocorrelations within the LH and testosterone time series, we filtered the data before subjecting them to the cross-correlation analysis. As a result, significant positive cross-correlations were found at a testosterone lag of 40 min in 10 peripubertal boys. We conclude that testosterone concentration profiles are pulsatile and show marked circadian rhythm well before the onset of puberty. LH and testosterone time series are significantly coupled when testosterone lags LH by about 40 min. This time lag might correspond to the time for synthesizing and secreting testosterone in Leydig cells after binding of LH to the Leydig cell receptors.

Adolescent↗