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PubMed1980

[Persistence of Muller's ducts in the male. A family observation (author's transl)].

The authors report two cases (in brothers) of the persistence of Muller's ducts (uterus and uterine tubes), whilst both individuals led a normal though infertile sex life. They presented with a bilateral inguinal hernia and a cryptorchidism. The precise diagnosis was made at surgery in the first, whilst the family history led to the diagnosis in the second. Both underwent bilateral orchidopexy, and hysterectomy with excision of the uterine tubes. The caryotypes were normal. Of anatomical interest was the fact that both had vas deferens included within the uterine wall but the there was no continuity between the epididymes and the testes. The latter contained seminiferous ducts, Sertoli cells and spermatogonia but no spermatocyte nor spermatozoa. On the basis of these cases, the authors emphasise their demonstrative nature: the presence of testes resulted by the secretion of testosterone in the induction of normal external genitalia whilst the absence of factor inhibiting Mullers ducts (or tissue resistance to this factor) resulted in the development of the uterine tubes and uterus.

Adult↗

PubMed1996

The regulation of adipose tissue distribution in humans.

The regulation of adipose tissue distribution is an important problem in view of the close epidemiological and metabolic associations between centralized fat accumulation and disease. With visceral fat accumulation multiple endocrine perturbations are found, including elevated cortisol and androgens in women, as well as low growth hormone (GH) and, in men, testosterone (T) secretion. These abnormalities probably derive from a hypersensitive hypothalamo-pituitary-adrenal axis, with hyperinsulinemia related to a marked insulin resistance as a consequence. These hormonal changes exert profound effects on adipose tissue metabolism and distribution. At the adipocyte level cortisol and insulin promote lipid accumulation by expressing lipoprotein lipase activity, while T, GH and probably estrogens exert opposite effects. The consequences will most likely be more expressed in visceral than subcutaneous adipose tissues because of a higher cellularity, innervation and blood flow. Furthermore, the density of cortisol and androgen receptors seems to be higher in this than other adipose tissue regions. The endocrine perturbations found in visceral obesity with an abundance of the lipid accumulating hormones cortisol and insulin, and a relatively low secretion of the lipid mobilizing sex steroid hormones and GH would therefore be expected to be followed by visceral fat accumulation. The potential significance of local synthesis of steroid hormones in adipose tissue requires more attention. Although studies in vitro are informative when elucidating detailed mechanisms of hormonal interactions, they might not give a true picture of the regional integrated regulation of adipose tissue lipid storage and mobilization. Such information can be obtained by regional measurements of lipid mobilization by free fatty acid turnover or by microdialysis techniques, both showing lower rates of mobilization in leg than in upper body adipose tissues. More detailed information can be obtained by physiological oral administration of triglycerides, labelled with a small amount of oleic acid, followed by measurements of the regional uptake and turn-over of adipose tissue triglycerides. Such studies show lipid uptake in the order omental = retroperitoneal > subcutaneous abdominal > subcutaneous femoral adipose tissues in men, with a similar rank order for half-life of the triglyceride, indicating also a turn-over of triglycerides in that order. T amplifies these differences in men. In premenopausal women subcutaneous abdominal has a higher turnover than femoral adipose tissue. Results of studies in vitro indicate that this difference is diminished at the menopause, and restored by estrogen substitution, suggesting that the functional effects of estrogens in women are similar to those of T in men. The mechanisms are, however, probably indirect because of the apparent absence of specific estrogen and progesterone receptors in human adipose tissue. This interpretation from the studies referred to above fits well with physiological, and clinical conditions with increased visceral fat mass, where the balance between the lipid accumulating hormone couple (cortisol and insulin) and the hormones which prevent lipid accumulation and instead activate lipid mobilization pathways (sex steroid hormones and GH) is shifted to the advantage of the former. Such conditions include Cushing's syndrome, the polycystic ovary syndrome, menopause, aging, GH-deficiency, depression, smoking and excess alcohol intake. With appropriate interventions against hypercortisolemia and substitution of deficient sex steroids and GH, visceral fat mass is decreasing. Based on this evidence from physiological, clinical, interventional observations and detailed studies of mechanisms at cellular and molecular levels it is suggested that the combined endocrine abnormalities in the syndrome of visceral obesity direct storage fat to visceral adipose depots. Therefore, measurements of visceral fat accumulat

Adipose Tissue↗

PubMed1997

Inhibition of bufalin on pituitary and testicular function in rats.

The effects of bufalin on the secretion of testosterone and luteinizing hormone (LH) and the accumulation of testicular adenosine 3':5'-cyclic monophosphate (cAMP) were studied. Male rats were injected with bufalin, human chorionic gonadotropin (hCG), gonadotropin releasing hormone (GnRH), hCG plus bufalin or GnRH plus bufalin via a jugular catheter. Blood samples were collected at several intervals subsequent to the challenge. In the in vitro study, rat testis blocks were incubated with bufalin, hCG or both for 1 h. The anterior pituitary gland was incubated with bufalin, GnRH or both for 30 min. The media were analyzed for testosterone or LH. For studying cAMP accumulation, testicular blocks were incubated for 1 h with the medium containing isobutyl-1-methylxanthine. After incubation, tissues were extracted by ethanol before measuring cAMP concentration. A single intravenous injection of bufalin decreased the basal and hCG-stimulated levels of plasma testosterone. Administration of bufalin in vitro resulted in an inhibition of both basal and hCG-stimulated release of testosterone. Bufalin diminished cAMP accumulation in rat testes. However, the basal levels of plasma and medium LH were not altered by bufalin administration. Likewise, the LH response to GnRH was diminished by bufalin administration, both in vivo and in vitro. These results suggest that the inhibition of testosterone production by bufalin is partly caused by a decrease of testicular cAMP accumulation and LH response to GnRH in rats.

1-Methyl-3-isobutylxanthine↗

PubMed1998

Studies on the effect of intratesticular administration of opioid peptides, naloxone or N-acetyl beta-endorphin antiserum on some testicular parameters in rats.

Opioid peptides have been localized in a variety of peripheral tissues like placenta, thyroid, pancreas, gastrointestinal tract, in the reproductive tract of male and female and in the testes of rats. Immunoassayable material was detected in extracts of gonads, reproductive tract and accessory reproductive organs. Studies with naloxone have suggested that beta-endorphin may have an important role in steroidogenesis and may have a role in regulating transport of luminal material. In our studies met-enkephalin, beta-endorphin, naloxone or N-acetyl beta-endorphin antiserum were microinjected intra testicularly once on alternate days for one week and autopsied 24 h after the last injection. Intratesticular administration of 25, 50 and 100 micrograms doses of naloxone induced significant decrease in in vitro secretion of testosterone per se, which was significantly greater with 50 micrograms dose than with those of the other two doses. A 25 micrograms dose had no effect on hyaluronidase or acid phosphatase activity while 50 micrograms dose significantly decreased the enzyme activity. One hundred micrograms dose also significantly decreased hyaluronidase activity. Intratesticular injection of 10 micrograms met-enkephalin or 1 microgram beta-endorphin significantly decreased hyaluronidase activity whereas 20 microliters N-acetyl beta-endorphin antiserum increased the specific activity of hyaluronidase. There was no change in the weight of the testes on treatment with the above agents.

Acid Phosphatase↗

PubMed1994

[Effects of cutaneous mechanical stimulation on plasma corticosterone, luteinizing hormone (LH), and testosterone levels in anesthetized male rats].

Effects of cutaneous mechanical stimulation on plasma corticosterone, luteinizing hormone (LH), and testosterone levels were examined in young adult (13-22 weeks old) and aged (24-27 months old) male Wistar rats anesthetized with pentobarbital. Under the resting condition without somatic sensory stimulation, neither plasma corticosterone measured every 15 min between 1430 h and 1630 h nor plasma LH and testosterone measured every 30 min between 1400 h and 1730 h revealed any significant fluctuations. Nociceptive mechanical stimulation of both hindpaws by pinching for 10 min significantly increased plasma corticosterone, LH, and testosterone, in young adult rats. Plasma corticosterone was increased for one hour following the stimulation. On the other hand, plasma LH was increased 30 and 60 min after the cessation of stimulation, while plasma testosterone was increased 60-150 min after stimulation. However, innocuous mechanical stimulation of both hindlimbs by brushing for 10 min did not significantly change either plasma corticosterone, LH, or testosterone. These findings indicate that, nociceptive information from skin lead to the increased secretion of corticosterone from the adrenal cortex and the increased secretion of LH from the anterior pituitary, resulting in an increase in testosterone secretion from the testes into the plasma, after emotional factors are eliminated by anesthetizing the subjects. In aged rats, the same nociceptive mechanical stimulation by pinching significantly increased the plasma corticosterone levels. The magnitude and time-course of the response in aged rats were equivalent to those in young adult rats. On the other hand, in aged rats, neither plasma LH nor testosterone levels were changed by the same nociceptive mechanical stimulation. This is in sharp contrast to the increase in both plasma LH and testosterone caused by the stimulation of young adult rats. These findings indicate a functional dissociation induced by aging between the secretory responses of the anterior pituitary, testes on the one hand and the adrenal cortex on the other hand, to nociceptive somatic sensory stimulation. Aging does not alter corticosterone release from the adrenal cortex to nociceptive somatic sensory stimulation, but LH secretion from the anterior pituitary and testosterone secretion from the testes to nociceptive somatic sensory stimulation are subject to dysfunction with aging.

Aging↗

PubMed2003

Valproate inhibits the conversion of testosterone to estradiol and acts as an apoptotic agent in growing porcine ovarian follicular cells.

PURPOSE: Long-term valproate (VPA) treatment has been associated with hyperandrogenism and polycystic ovaries in women with epilepsy. The exact mechanisms of action of the drug on sex steroid hormone function are still unsettled. The aim of the present study was to investigate the action of VPA on basal and gonadotropin-stimulated steroid secretion in porcine ovarian follicular cells and to measure the conversion of testosterone to estradiol. Second, the action of VPA on proliferation and apoptosis of follicular cells was investigated. METHODS: Small and medium follicles were obtained from pig ovaries on days 8-10 and 14-16 of the estrus cycle. Both follicular compartments, theca and granulosa cells, were cultured as a coculture resembling follicles in vivo. VPA in concentrations of 100 and 250 micrg/ml was added to the control or gonadotropin-stimulated cultures. RESULTS: VPA caused a significant increase in basal and luteinizing hormone (LH)-stimulated testosterone secretion from small follicles, whereas in medium follicles, an increased basal but decreased LH-stimulated testosterone secretion was found. VPA caused decreased basal and follicle-stimulating hormone (FSH)-stimulated estradiol secretion by small follicles, whereas only the higher concentration decreased estradiol secretion in medium follicles. The conversion of testosterone to estradiol by small follicles was decreased under the influence of VPA in testosterone-alone and in testosterone-plus-FSH-stimulated cultures, whereas this was seen at only the higher VPA concentration in medium follicles. VPA had no effect on cell proliferation and viability, whereas in a dose-dependent manner, VPA increased caspase-3 activity. CONCLUSIONS: VPA affected steroidogenesis in both unstimulated and gonadotropin-stimulated porcine ovarian follicular cells and inhibited the conversion of testosterone to estradiol. In addition, VPA may act as an apoptotic agent in both small and medium-sized follicles.

Animals↗

PubMed1999

Total testosterone and DHEAS levels as predictors of androgen-secreting neoplasms: a populational study.

Androgen excess affects between 2% and 10% of women. While the majority of these patients suffer from polycystic ovary syndrome, a few present with an androgen-secreting neoplasm. An elevated circulating total testosterone level and dehydroepiandiosterone sulfate (DHEAS) level have been proposed as screening methods for detecting ovarian and adrenal androgen-secreting neoplasms, respectively. To determine the predictive value of these tests for androgen-secreting tumors in a population of consecutive hyperandrogenic patients, we studied 478 consecutive untreated hyperandrogenic patients presenting over a ten-year period (1987-97). All had at least two of the following features: (1) oligomenorrhea (i.e. cycles > 35 days or < 8 cycles/year), (2) hyperandrogenemia (i.e. a total or free testosterone, or DHEAS > 95th percentile of controls), or (3) hirsutism (i.e. a modified Ferriman-Gallwey score > or = 6). None of these patients had a prior diagnosis of an androgen-secreting neoplasm. Basal levels of testosterone and DHEAS were determined in all patients, with transvaginal sonography and an adrenal computed tomography scan in select individuals. Of the 478 patients included, 65% had hirsutism and oligomenorrhea; 20% had hyperandrogenic oligomenorrhea; and 15% had hirsutism and hyperandrogenemia, without overt oligomenorrhea. Overall, 11 (2.3%) patients had a total testosterone > 8.7 nmol/l (250 ng/dl), of which one actually had an androgen-secreting neoplasm (i.e. true-positive). This postmenopausal patient presented with rapidly progressive virilization, and demonstrated an ovarian hilar cell tumor at surgery. The calculated sensitivity of an elevated testosterone level (> 8.67 nmol/l) for a neoplasm was 100% (1/1), the specificity was 98% (467/477), and the negative predictive value was 100% (467/467), but the positive predictive value was only 9% (1/11). Ten subjects had DHEAS levels > 16.3 mumol/l (6000 ng/ml), and none was diagnosed with an adrenocortical tumor. Although the sensitivity and positive predictive value of a high DHEAS for a neoplasm could not be calculated due to the absence of a test case, the specificity was 98% (468/478) and the negative predictive value was 100% (468/468). These data suggest that the measurement of testosterone and DHEAS is not a cost-effective method of screening for these tumors, due to the low frequency of the disorder and the fact that clinical evaluation alone is often sufficient screening.

Adrenal Cortex Neoplasms↗

PubMed1994

Secretion pattern of immunoreactive inhibin in men.

Chronological changes in serum concentrations of inhibin, a gonadal glycoprotein hormone, were studied in healthy male volunteers (age 24-27 years). Secretion profiles of immunoreactive inhibin (ir-inhibin) were compared with those of luteinizing hormone (LH), follicle-stimulating hormone (FSH) and testosterone. Blood samples were collected every 15 min for 24 h. Serum inhibin concentrations were measured by a two-site immunoenzymatic assay with antibodies raised against distinct epitopes of the recombinant 1-32 amino acids of the alpha-subunit of human inhibin. The normal range for men was 0.79-3.1 U/l x 10(-3), the sensitivity of the assay was 0.1 U/l x 10(-3) (cv: within-assay, 6.8%; between-assay, 8.2%). Luteinizing hormone and FSH were measured by immunoradiometric assay and testosterone by radioimmunoassay. Secretion profiles of inhibin and testosterone were tested for diurnal variations by cosinor rhythmometry. Highest ir-inhibin concentrations were observed in the morning at 08.00 h, with peak values of 2.45-3.20 U/l x 10(-3). During the evening and the night, ir-inhibin levels were relatively low; lowest concentrations were observed between 01.00 h and 02.00 h at night: 1.20-1.86 U/l x 10(-3). Highest testosterone levels were observed in the morning (20.5-36.6 pmol/l), lowest concentrations were detected at night (7.35-12.6 pmol/l). Cosinor rhythmometry supported the suggestion that there is a clear circadian secretion of ir-inhibin and testosterone, respectively. The secretion pattern of ir-inhibin was analyzed by the Cluster pulse analysis computed algorithm, which identified four to seven inhibin pulses per day, depending on the person under observation.2+ volunteers follow a clear diurnal rhythm.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1985

Imprinting of growth hormone secretion, body growth, and hepatic steroid metabolism by neonatal testosterone.

The influence of endogenous sex steroids and exogenous testosterone treatment on pulsatile GH secretion, body weight, longitudinal bone growth, and hepatic steroid metabolism was studied in male and female adult rats. Blood samples were obtained from the tip of the tail, and maximum and minimum GH levels were determined in individual rats to evaluate pulse heights and baseline levels. Longitudinal bone growth was measured using the intravital marker tetracycline, and hepatic steroid metabolism was evaluated by determining the enzyme activities of 16 alpha-hydroxylase and 5 alpha-reductase. Neonatal, but not prepubertal, gonadectomy of male rats suppressed maximum and mean plasma GH levels during adult life. The body weight and the rate of longitudinal bone growth were also decreased. Testosterone treatment neonatally reversed all of these effects. Neonatal gonadectomy of male rats also caused an elevation of minimum plasma GH levels, an effect, however, which was not reversed by testosterone replacement during neonatal life. Neonatally gonadectomized females treated with testosterone neonatally or during adult life increased their maximum and decreased their minimum GH levels. Their longitudinal bone growth was increased. The body weight of these rats was increased by neonatal, but not adult, testosterone treatment. There was no effect of neonatal ovariectomy on plasma GH levels in 3- to 4-month-old female rats. However, neonatal ovariectomy did increase the maximum and mean plasma GH levels immediately postpubertally, suggesting that the effect of the ovaries on GH secretion differs among mature female rats of different ages. Prepubertal gonadectomy of male rats feminized their hepatic steroid metabolism by decreasing 16 alpha-hydroxylase and increasing 5 alpha-reductase activities. Neonatal gonadectomy caused an even more pronounced feminization, which was partly reversed in rats given testosterone replacement therapy neonatally. In neonatally gonadectomized female rats, treatment with testosterone during adult life increased 16 alpha-hydroxylase and decreased 5 alpha-reductase to levels seen in intact male rats. The present results indicate that neonatally secreted testicular androgens imprint the high amplitude pulses characteristic of GH secretion in adult male rats. Neonatal androgens also stimulate somatic growth and partially account for the masculinized hepatic steroid metabolism in the adult animal. It is proposed that imprinting of the GH secretory pattern contributes to the influence of neonatal testicular androgens on body growth and hepatic steroid-metabolizing enzymes.

Animals↗

PubMed1996

'Hamster-like' cycles in testicular size in the absence of gonadotrophin secretion in HPD rams exposed to long-term changes in photoperiod and treatment with melatonin.

Long term changes in the secretion of FSH, LH and testosterone, and the size of the testis were measured in groups of hypothalamo-pituitary disconnected Soay rams (HPD rams, n = 8) and control Soay rams (HPD-sham operated and unoperated, total n = 8) while exposed to an artificial lighting regimen of alternating 16-weekly periods of long days (16L: 8D) and short days (8L: 16D), and when treated with a constant-release implant of melatonin given under long days (total study: 136 weeks). Short term provocation tests using NMDA (glutamate receptor agonist), GnRH and LH were used to assess functionality of the hypothalamus, pituitary gland and testis, respectively. Control rams expressed normal photoperiod-induced cycles in the reproductive axis. Blood concentrations of FSH, LH and testosterone were significantly increased under short days, and decreased under long days with parallel changes in testicular diameter. Treatment with implants of melatonin under long days mimicked the effect of short days and induced rapid reactivation of the reproductive axis. In the HPD rams the blood concentrations of FSH, LH and testosterone declined immediately after the HPD surgery and values remained close to the lower limit of detection of the radioimmunoassays throughout the experiment. LH pulses were absent in the HPD rams and NMDA failed to induce LH secretion consistent with functional disconnection of the pituitary gland from the hypothalamus. The testes regressed to a significantly smaller size in the HPD rams compared with controls even at the nadir of the sexual cycle (testis diameter: 30.2 +/- 0.7 vs 41.3 +/- 0.8 mm, HPD vs control rams, respectively). A low amplitude cycle in testicular diameter (peak to nadir: 5.0 +/- 0.7 mm) persisted in the HPD rams with a temporal pattern opposite to the controls (growth under long days instead of short days; 'hamster like'). In the HPD rams, the treatment with melatonin blocked the long day-associated increase in testicular size, without effects on FSH, LH and testosterone secretion, pituitary responsiveness to GnRH (LH increment) or testicular responsiveness to LH (testosterone increment). This was in contrast to the cyclical changes in all parameters induced by melatonin in the control rams. At post-mortem, the reproductive tract in HPD rams was markedly regressed compared with the controls. The efficiency of spermatogenesis was reduced with few germ cells maturing beyond primary spermatocytes. Immunocytochemical staining, however, revealed the maintenance of androgen receptor expression in Sertoli cells, pertibular cells and Leydig cells, and steroid activity as measured by 17 alpha-hydroxylase expression in Leydig cells. Overall, the absence of photoperiod-induced changes in gonadotrophin secretion in the HPD rams illustrates the dependence on regulation by the hypothalamus, presumably through the secretion of GnRH. The residual cycle in the size of the testes in the HPD rams was closely correlated with the photoperiod-induced changes in prolactin secretion which persisted in these animals (summary of previous published data included). The combined results support the view that melatonin acts in the hypothalamus to mediate effects of photoperiod on gonadotrophin secretion and in the pituitary gland to mediate effects on prolactin secretion (dual site hypothesis), and that FSH, LH and prolactin act synergistically to regulate the long-term cycle in testicular activity in the ram.

Animals↗

PubMed1992

Nitric oxide control of steroidogenesis: endocrine effects of NG-nitro-L-arginine and comparisons to alcohol.

Recent studies suggest that nitric oxide (NO) may regulate hormone biosynthesis and secretion. This was tested by treating male rats with NG-nitro-L-arginine methyl ester (NAME), a NO synthase inhibitor, and measuring serum and testicular interstitial fluid testosterone and serum corticosterone, luteinizing hormone (LH), and prolactin (PRL). The effect of NG-nitro-L-arginine (NA), a less-soluble form of the same NO synthase inhibitor, on the reproductive suppressant actions of alcohol was also examined. NAME increased testosterone and corticosterone secretion dose-dependently without affecting LH and PRL secretion. The alcohol-induced suppression of testosterone or LH secretion was not altered by treatment with NA. Although effects of NAME and NA on other systems may be involved, these results indicate that testicular and adrenal steroidogenesis are negatively regulated by endogenous NO and that NO does not regulate LH and PRL secretion or inhibit the testicular steroidogenic pathway in the same way as alcohol.

Analysis of Variance↗

PubMed2004

Erosion of endogenous testosterone-driven negative feedback on pulsatile luteinizing hormone secretion in healthy aging men.

The present study tests the intuition that successful aging in men is marked by: 1) impaired feedforward by endogenous LH concentrations (con) of testosterone (Te) secretion (sec); and/or 2) attenuated feedback by unmanipulated Te con of LH sec. The goal was to assess both implicit linkages analytically without disrupting normal pathway coupling. This strategy required: 1) assay of paired LH and Te con sampled every 10 min for 24 h in 13 older (O) (ages 60-78 yr) and 13 young (Y) (ages 18-30 yr) men; 2) deconvolution-based estimation of LH and Te sec rates; 3) lag-specific cross-correlation analyses of the relationships between LH and Te con and sec; and 4) statistical contrasts by age stratum. Salient outcomes were: 1) O and Y men maintain comparable LH con drive of Te sec, viz maximal r = +0.51 and r = +0.52, respectively, at an optimal time lag of 50 min (both P < 0.001 against random LH and Te associations); 2) elderly subjects exhibit reduced Te con inhibition of LH sec [minimal r = -0.008 (O) vs. r = -0.10 (Y), P < 0.01 at a time lag of 40 min]; 3) mean (24-h) LH con do not differ by age; and 4) molar Te/sex hormone-binding globulin con are lower in the elderly than in Y individuals (P < 0.01).In conclusion, noninvasive analyses predict that attenuation of endogenous Te feedback restraint on the hypothalamo-pituitary unit may be an early biological marker of adaptive changes in the GnRH-LH-Te ensemble axis in the healthy O male.

Adolescent↗

PubMed1996

Effect of a specific aromatase inhibitor on oestradiol secretion by porcine corpora lutea at various stages of the luteal phase.

The present study was undertaken to investigate the aromatization capability of pig corpora lutea at different stages of the luteal phase using the nonsteroidal aromatase inhibitor CGS 16949A. Luteal cells were collected during early (0-2 days after ovulation), mid- (7-10 days after ovulation) and late (13-16 days after ovulation) luteal phase. Cells were incubated either with or without 10(-7) MT (testosterone-supplemented culture). Six hours after starting the cultures, 0.1, 0.5 or 1.0 microM aromatase inhibitor was added to both culture types for the next 12 h period. Addition of the aromatase inhibitor to the luteal cells isolated during the early luteal phase had no effect on basal and testosterone-supplemented oestradiol secretion. The aromatase inhibitor added to cells isolated during the mid- and late luteal phase, however, caused a significant decrease in the basal and testosterone-stimulated secretion of oestradiol. This supports the hypothesis that luteal cells from these stages have active aromatase. The highest aromatization potential was observed in regressing corpora lutea. Oestradiol secreted by the regressing corpora lutea could play an active role in the regulation of oestrus cycle and could have a possible endocrine influence on gonadotropin secretion, a paracrine action on follicular growth or an autocrine influence on the luteal activity.

Animals↗

PubMedDate not supplied

[Effect of corticoliberin and naloxone on the functional activity of the hypophyseal-gonadal system in monkeys].

Experiments were staged on male Papio hamadryas for a study of CRF and naloxone action on the time course of LH and testosterone in peripheral blood. LH was determined by a biological micromethod in vitro; ACTH, cortisol and testosterone were determined by radioimmunoassays. Exogenous CRF was shown to increase inhibitory action of acute "procedure" stress (frequent fixation of monkeys and venipuncture for taking blood samples) of the secretion of LH but not testosterone. Opioid preceptor blockade with naloxone prevented the appearance of inhibitory action of stress and CRF on hypophyseal gonadotropic function rather than on testicular secretory activity. The time course of LH and testosterone after naloxone administration of naloxone combined with CRF has shown that inhibition of testosterone secretion in stress does not depend on a response of gonadotropins and is determined by other (additional) factors.

Adrenocorticotropic Hormone↗

PubMed1988

Mechanism of action of the factor(s) secreted by rat seminiferous tubules and inhibiting interstitial cell testosterone production in vitro.

Rat seminiferous tubules secrete a factor which inhibits LH-dependent steroidogenesis by interstitial cells. The inhibitory activity was found to be specific for the testes, as cytosols from other rat tissues such as the kidney, heart, spleen, liver and epididymis had no significant effect on testosterone production by interstitial cells. Preliminary characterization by Ultrogel AcA 44 gel chromatography demonstrated that the active substance in SMST has a molecular weight between 40-50 kD. Spent medium from incubation of seminiferous tubules (SMST) caused a dose-dependent inhibition of LH-or cholera toxin-stimulated in vitro testosterone production by rat interstitial cells. However, SMST failed to inhibit forskolin-stimulated steroidogenesis. The effect of SMST was not altered by pre-incubating the cells with the sulfhydryl reagent, N-ethylmaleimide. Considering the proposed mode of action of these modulators of adenylate cyclase activity, the present studies suggest that a high molecular weight testis specific factor acts through the guanine nucleotide-binding stimulatory regulatory protein of the adenylate cyclase complex to inhibit LH-dependent testosterone production by Leydig cells.

Animals↗

PubMed1989

The effects of long term testosterone administration on pulsatile luteinizing hormone secretion and on ovarian histology in eugonadal female to male transsexual subjects.

Polycystic ovarian disease (PCOD) is associated with elevated serum LH and (sub)normal FSH levels, while serum androgen levels are often elevated. To clarify the role of androgens in this abnormal pattern of gonadotropin secretion, LH secretion was studied in 1) 9 eugonadal female to male transsexual subjects before and during long term (6 months) testosterone (T) administration (250 mg/2 weeks, im), and 2) in a woman with an androgen-secreting ovarian tumor both before and after surgical removal of the tumor. Finally, we studied the effects of high serum androgen levels on ovarian histology in 3) 26 transsexual subjects after long term (9-36 months) T administration (250 mg/2 weeks, im) to assess whether T-induced ovarian abnormalities are similar to those that occur in women with PCOD. Long term T treatment in the nine female to male transsexual subjects resulted in increases in the mean serum T level from 1.7 +/- 0.8 (+/- SD) to 40.8 +/- 31.9 nmol/L (P less than 0.01), the mean serum dihydrotestosterone level from 0.6 +/- 0.2 to 3.3 +/- 1.5 nmol/L (P less than 0.02), and the mean serum free T level from 9.5 +/- 5.2 to 149 +/- 46 pmol/L (P less than 0.02). Mean serum estrone and estradiol levels were similar before and during T treatment. The mean serum LH level decreased from 6.3 +/- 2.0 to 2.9 +/- 1.1 U/L (P less than 0.01), and the mean FSH levels decreased from 6.6 +/- 2.0 to 3.7 +/- 2.2 U/L (P less than 0.02). Pulsatile LH secretion before and during T treatment was studied in five subjects. Neither the mean nadir LH interval nor the LH pulse amplitude changed significantly in these five subjects. The serum T level in the woman with the androgen-secreting ovarian tumor was 9.6 nmol/L, and it declined to normal after removal of the tumor. Her mean serum LH and FSH levels, the mean nadir LH interval, and LH pulse amplitude were in the normal range before and after removal of the tumor. Studies of ovarian histopathology in 26 transsexual subjects after long term androgen treatment revealed multiple cystic follicles in 18 subjects (69.2%), diffuse ovarian stromal hyperplasia in 21 subjects (80.8%), collagenization of the tunica albuginea in 25 subjects (96.2%), and luteinization of stromal cells in 7 subjects (26.9%). Findings consistent with criteria for the pathological diagnosis of polycystic ovaries, that is 3 of the 4 findings listed above, were present in 18 of the 26 subjects (69.2%).(ABSTRACT TRUNCATED AT 400 WORDS)

Androgens↗

PubMed1982

Influence of 2 Br-alpha-ergocryptine (CB 154) on the secretion of prolactin, LH, FSH and testosterone and on testicular growth in rams subjected to different photoperiods.

The influence of 2-Br-alpha-ergocryptine (CB 154) on the secretion of gonadotrophins and on testicular function has been studied in rams subjected to either a normal photoperiod or an abnormal photoperiod causing hyperprolactinaemia. The CB 154 treatment significantly lowered the mean frequency of LH and testosterone pulses in hyperprolactinaemic animals as compared to solvent-treated ones. Also, only those groups subjected to an abnormal photoperiod (groups 2 and 3) exhibited a significant rise in the frequency of LH and testosterone peaks after CB 154 was withdrawn. During treatment, plasma FSH concentrations increased significantly only in group 1 which was subjected to normal photoperiodic variations. Testicular growth was delayed in CB 154-treated rams compared to solvent-treated ones only in group 3 (hyperprolactinaemic).

Animals↗

PubMed1994

The effect of changing gonadotropin-releasing hormone pulse frequency on puberty.

We have examined the effect of using different pulse frequencies of exogenous GnRH to induce puberty and the time relationship among LH, FSH, sex steroids, and GH in these individuals. Five girls and three boys with delayed puberty received exogenous GnRH at either 3-h frequency (slow) or every 45 min (fast). Treatment was initially given overnight and increased to 24 h when breast stage 3 in girls or testicular volume of 10 mL in boys was attained. Twenty-four-hour gonadotropin profiles were performed after 5 days, 1 month, 3 months, 6 months, and 1 yr of treatment. Temporal relationships among LH, FSH, and estradiol; LH and testosterone; GH and estradiol; and GH and testosterone were examined by cross-correlation. There was no difference in the rate of pubertal progress between the groups. Mean serum gonadotropin and sex steroid levels did not differ. LH was correlated with estradiol for both groups at 240 min (slow group, r = 0.54; fast group, r = 0.50). Estradiol correlated with LH at 300 min in the slow group (r = -0.41) and 200 min in the fast group (r = -0.37). FSH correlated with estradiol at 140 min in the slow group (r = 0.62) and 160 min in the fast group (r = 0.50). A rise in estradiol occurred 140-160 min after a rise in FSH and 240 min after a rise in LH. A rise in estradiol was followed 200-300 min later by a fall in LH. LH was correlated with testosterone at 60 min in the slow group (r = 0.73) and at 40 min in the fast group (r = 0.55). Testosterone correlated with LH at 420 min in the slow (r = -0.67) and 460 min in the fast group (r = -0.40). A rise in LH was followed 40-60 min later by a rise in testosterone. A rise in testosterone was followed by fall in LH 420-460 min later. GH correlated with estradiol at 320 min in the slow group (r = 0.37) and 380 min in the fast group (r = 0.38). A rise in GH was followed, after 320-380 min, by a rise in estradiol. There was a correlation between GH and testosterone in the slow group after 280 min (r = 0.44). A rise in GH was followed by a rise in testosterone after 280 min. The pituitary-gonadal axis is sufficiently robust to allow puberty to progress with different fixed pulse frequencies. There is a temporal relationship among LH, FSH, and estradiol secretion and between LH and testosterone secretion. We have demonstrated the feedback effect of sex steroids at the level of the pituitary and the time course of the effect of GH on gonadal function.

Adolescent↗