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PubMed1999

Central administration of corticotrophin releasing hormone but not arginine vasopressin stimulates the secretion of luteinizing hormone in rams in the presence and absence of testosterone.

This study tested the hypothesis that central administration of corticotrophin-releasing hormone (CRH) and/or arginine vasopressin (AVP) will affect the secretion of LH in rams and that testosterone is necessary for these actions to occur. Plasma LH levels were measured in castrated rams during 1 h infusion of either 100 microliter vehicle/mock cerebrospinal fluid (CSF) or mock CSF containing 25 microgram CRH, 25 microgram AVP or 25 microgram of each peptide through guide cannulae into the third cerebral ventricle. These intracerebroventricular (i.c.v.) infusions were given to the castrated rams following injections (i.m.) each 12 h of oil or 8 mg testosterone propionate for 7 days. Blood samples were collected every 10 min for 4 h before i.c.v. infusion, during infusion and for 4 h following the infusion. Infusion of vehicle did not affect any endocrine parameters. In contrast, the plasma concentrations of LH and the amplitude of LH pulses were increased significantly during and following infusion of CRH, and this effect was not influenced by whether the castrated rams were treated with testosterone propionate or whether the CRH was administered in combination with AVP. Infusion of AVP alone did not affect LH secretion. The frequency of LH pulses and the plasma concentrations of FSH did not change with any of the i.c.v. treatments. The plasma concentrations of cortisol were significantly increased by CRH and AVP infusions. The plasma concentrations of cortisol achieved during and following i.c.v. infusion of CRH and AVP combined were greater than the concentrations achieved as a result of treatment with AVP alone but were similar to those with CRH. There was no effect of testosterone propionate on cortisol levels. These results show that CRH, but not AVP, is capable of acting either centrally or at the pituitary level to increase the secretion of LH in rams and these actions are not affected by testosterone. The stimulatory effects of CRH on LH secretion are to increase the amplitude of GnRH pulses and/or the responsiveness of the pituitary to the actions of GnRH with no effect on the frequency of GnRH pulses. The secretion of FSH in rams is not influenced by either CRH or AVP. The effect of CRH to increase LH pulse amplitude occurs in the face of increased cortisol levels, further reinforcing our belief that this adrenal steroid does not affect the reproductive axis in this species.

Animals↗
PubMedDate not supplied

[Hormonally-active ovarian tumors in 30 years of data (1965-1994)].

INTRODUCTION: Authors have investigated the incidence and distribution of hormonally active ovarian tumors in a 30-year surgical material. Out of 552 ovarian tumors, there were 28 hormonally active tumors (5.07%): 18 granulosa cell tumors, 4 thecomas, 2 arrhenoblastomas, 2 malignant v. Kalden folliculomas. There were laso 2 benign tumors: ectopic adrenal ovarian tumor, and ovarian tube hydatidiform mole. They secrete estrogen and testosterone and their effects are evident: prior to puberty (Praecox pubertas), during the reproductive period, but most often in menopause. In order to make the diagnosis, when uterine hemorrhage occurs, it is necessary to perform explorative curettage, but the tumors must be surgically removed. It is necessary to perform that kind of surgery, which corresponds to the age of the woman. Recurrences may appear even 35 years later. MATERIAL AND METHODS: Hysterectomy with bilateral adnexectomy was performed in 18 (64.28%) postmenopausal women. In 4 (14.29%) women of reproductive age unilateral adnexectomy was performed, while explorative laparotomy was performed also in 4 (14.29%) women. 5-year survival in the first stage of the disease was 75% (20 women). During the first three years 5 (17.86%) women decreased in the IV stage of the disease, as well as one woman (3.57%) in the II b stage, which makes a total of 6 women (21.43%) with fatal outcome. Ovarian tumors also include hormonally active tumors which secrete female and male sex hormones, and whose effects are evident on hormonal receptors. They are divided into benign or malignant, whereas they are all potentially malignant. We differentiate two groups: 1. Feminizing mesenchymomas, which secrete female sex hormones and 2. Virilizing tumors, which secrete male sex hormones. These tumors may occur prior puberty, during the reproductive period and in the postmenopausal period--senium. They can cause minor, long-term or hemorrhages similar to menstruation, as well as hypertrophy of the myometrium. Glandular cystic hyperplasia occurs often, whereas proliferation is rare. Histopathological findings after surgery (for example of myoma) are often surprising, because they reveal hormonally active undetected ovarian tumors or glandular cystic endometrial hyperplasia. All hormonally active tumors are potentially malignant. The aim of this retrospective study was to compare our prior attitudes and interventions with newer attitudes and to make changes on behalf of our patients. RESULTS: Our investigation included 552 adnexal tumors in a 30-year material. Each woman with uterine hemorrhage had undergone explorative curettage and the material was sent for histopathological analysis. During the investigated period 28 hormonally active tumors were found: 2 benign and 26 malignant or potentially malignant tumors (Table 2). There were 18 cases (40.91%) with granulosa cell tumors, 6 cases (13.64%) with cystadenocarcinoma ovarii serosum; 3 cases (6.82%) with borderline tumors; 4 cases (9.09%) with thecoma of the ovarii. Pseudomucious adenocarcinoma was found in 2 cases (4.55%) as well as endometrial adenocarcinoma, malignant mesenchymoma, arrhenoblastoma, malignant folliculoma v. Kalden; whereas malignant teratoma was established in 1 case (2.27%), as well as anaplastic carcinoma, metastatic carcinoma--Krunberg. It is obvious that hormonally active tumors make almost half of the cases (46.43%) and occur mostly at the age of 50-59 years of age (3.4%). Out of 28 patients, 18 underwent hysterectomy and bilateral adnexectomy (64.28%); 4 (14.29%) underwent unilateral adnexectomy that is explorative laparotomy for taking bioptic samples for histological examination (14.29%). Out of 28 patients, 4 were women of reproductive age. All of them underwent adnexectomy and are alive. Hemorrhages usually occur a few years after menopausal period. In one case it occurred 35 years after menopause (arrhenoblastoma), in another 25 years after menopause due to endometrial carcinoma asso

Adult↗
PubMed2002

Androgens decrease plasma adiponectin, an insulin-sensitizing adipocyte-derived protein.

Adiponectin, an adipose-specific secretory protein, exhibits antidiabetic and antiatherogenic properties. In the present study, we examined the effects of sex hormones on the regulation of adiponectin production. Plasma adiponectin concentrations were significantly lower in 442 men (age, 52.6 +/- 11.9 years [mean +/- SD]) than in 137 women (53.2 +/- 12.0 years) but not different between pre- and postmenopausal women. In mice, ovariectomy did not alter plasma adiponectin levels. In contrast, high levels of plasma adiponectin were found in castrated mice. Testosterone treatment reduced plasma adiponectin concentration in both sham-operated and castrated mice. In 3T3-L1 adipocytes, testosterone reduced adiponectin secretion into the culture media, using pulse-chase study. Castration-induced increase in plasma adiponectin was associated with a significant improvement of insulin sensitivity. Our results indicate that androgens decrease plasma adiponectin and that androgen-induced hypoadiponectinemia may be related to the high risks of insulin resistance and atherosclerosis in men.

3T3 Cells↗
PubMed2005

Central hormonal regulation and dimorphism of arousal.

From studies in animals, we have learned that differences in sexual behaviour between males and females reflect anatomical and biochemical differences between the male and female brain. A masculine behaviour (and therefore a masculine brain) results from the biological effect on the developing brain exerted by testosterone, which is secreted by the gonads and aromatized into oestrogens in the brain. However, congenital disorders of the androgen as well as oestrogen signalling in human males have failed to show any appreciable derangement in sexual behaviour. Based on other evidence in animals, sexual differences in brain (and behaviour) are not hormonally triggered but genetically determined. This other theory states that sexual behaviour is determined by the chromosomal sex existing in cells, including brain cells. A number of excitatory and inhibitory signals modulate the activity of certain brain structures. Scientists have begun to test some of these chemicals or their synthetic analogues/antagonists in humans.

Animals↗
PubMed2005

Infertility in the dromedary bull: a review of causes, relations and implications.

Research into infertility in the dromedary bull, as reported during the last two decades, is reviewed with emphasis on causes and effects. Reproductive activity of such animals is naturally limited by a breeding season, though with enough encouragement some may mate with oestrous females out of season but a full fertilization potential can in no way be expected. It is essential that any female presented to a bull is capable of reproducing. The presentation of a subfertile or infertile female due to infection or physiological abnormality will adversely affect the female's ability to conceive and, therefore, the apparent fertility rates of the bull she was put to. The average number of successful services a bull could be expected to perform is two per day. Dromedary bulls with large testes have larger sperm outputs and can cope with more than two females per day providing that they are given adequate periods of rest, 1-2 days every 10 days or so, in conjunction with appropriate nutrition throughout the season. Anabolic steroids or testosterone therapies, which are sometimes used in an attempt to improve male characteristics and bull libido, are not recommended for dromedary bulls in breeding work. Such steroids result in a decrease in testicular size and weight with fewer sperm per gram of testicular tissue being found and the sperm produced also have lower motility rates. Pain associated with the act of mating a she-camel, due to injuries or inflammation in the scrotum, testes, prepuce and sheath, can cause a permanent reduction in bull libido. Camel bulls achieving pregnancy rates more than 60% have had consistently higher spermatozoal concentrations and kinematic variables derived by the computerized cell motion analyzer (CMA) system. As far as physical capabilities are concerned, 3-year-old dromedary bulls, which have reached puberty, have been shown to be perfectly capable of fertilizing a female, but they have a limited sperm production to perform consistently throughout the season in a large herd. By 4.5-5.0 years of age, they are capable of producing adequate numbers of sperm to mate as many as females as an adult bull but fertilizing capacity is not attained until 6 years of age on average. Hyperoestrogenaemia, associated with autoimmune thyroiditis and trypanosomiasis, suppresses the secretion of testicular testosterone and augments the release of testicular histamine, which appears mandatory for quantitative reduction/loss of advanced spermatogenic cells in infertile dromedary bulls.

Aging↗
PubMed2000

Male hypogonadism caused by homozygous deletion of exon 10 of the luteinizing hormone (LH) receptor: differential action of human chorionic gonadotropin and LH.

We report the unique case of a patient with Leydig cell hypoplasia (LCH) type II caused by a genomic deletion resulting in the complete absence of exon 10 of the LH receptor (LHR). The patient presented at the age of 18 yr with retarded pubertal development, small testicles, and delayed bone maturation. LH was highly elevated, with very low serum testosterone levels. Genetic analysis revealed a homozygous deletion of approximately 5 kbp encompassing exon 10 of the LHR gene. Screening of family members demonstrated heterozygosity for the deletion, indicating autosomal recessive inheritance. At the time of examination, the patient displayed nearly normal male phenotype, but lacked pubertal development and was hypogonadal. Obviously, fetal male development sustained by hCG was normal, whereas LH action, important for pubertal development, was impaired. A hCG stimulation test induced testosterone biosynthesis and secretion within the normal range. Subsequently, hCG treatment was continued, resulting in an increase in testicular volume and the appearance of spermatozoa in the ejaculate after 16 weeks of treatment (5.3 million/mL). Despite highly elevated endogenous LH serum levels, the response to hCG indicates a possible dual mechanism of hormone binding and signal transduction for hCG and LH on a LHR that lacks exon 10. Furthermore, this patient represents the clinical counterpart of the normal male marmoset monkey (Callithrix jacchus), in which the expressed LHR lacks exon 10 in toto. This case provides important clinical insights about the possible role of exon 10 of the LHR in discriminating between LH and hCG actions.

Adolescent↗
PubMed2002

The neuroendocrinology of human puberty revisited.

The fundamental aspects of the hypothalamic luteinizing hormone-releasing hormone (LHRH)(1) [1]pulse generator-pituitary gonadotrophin-gonadal apparatus in mammals have striking commonalities. There are, however, critical, substantive differences in the neuroendocrinology of puberty among species. The onset of puberty in the human is marked by an increase in the amplitude of LH pulses, an indirect indicator of the increase in amplitude of LHRH pulses. The hypothalamic LHRH-pituitary gonadotrophin complex is functional by at least 0.3 gestation in the human foetus; the sex difference in the fetal and neonatal pattern of LH and FSH secretion is an apparent consequence of imprinting of the fetal hypothalamus-pituitary-gonadotropin apparatus by fetal testosterone. Until about 6 months of age in boys and 12-24 months in girls, the testes and ovaries respond to the increased LH in boys and follicle-stimulating hormone (FSH) in girls by secreting testosterone and oestradiol, respectively, reaching levels that are not again achieved before the onset of puberty. Striking features of the ontogeny of the human hypothalamic pulse generator are: (1) its development and function in the foetus; (2) the continued function of the hypothalamic LHRH pulse generator-pituitary gonadotrophin-gonadal axis in infancy; (3) the gradual damping of hypothalamic LHRH oscillator activity during late infancy; (4) its quiescence during childhood - the so-called juvenile pause; (5) during late childhood the gradual disinhibition and reactivation of the LHRH pulse generator, mainly at night; (6) the increasing amplitude of the LHRH pulses, which are reflected in the progressively increased and changing pattern of circulating LH pulses, with the approach of and during puberty. The intrinsic central nervous system (CNS) mechanisms responsible for the inhibition of the LHRH pulse generator during childhood (the juvenile phase) involve the major role of an inhibitory neuronal system - the CNS inhibitory neurotransmitter gamma-aminobutyric acid (GABA) and GABAergic neurons, as revealed by studies in the rhesus monkey by Terasawa and her associates. With the onset of puberty, the disinhibition and reactivation of the LHRH pulse generator is associated with a fall in GABAergic neurotransmission and a concomitant increase in the input of excitatory amino acid neurotransmitters (including glutamate) and possibly astroglial-derived growth factors. Despite remarkable progress over the past three decades, large gaps remain in our understanding of the neurobiological, genetic and environmental mechanisms involved in the control of the onset of puberty. The role of leptin in the control of the onset of puberty is reviewed. Severe leptin deficiency is associated with hypogonadotrophic hypogonadism; it appears that a critical level of leptin and a leptin signal is required to achieve puberty. The weight of evidence supports the hypothesis that leptin acts as one of several permissive factors and not a trigger in the onset of human puberty. The application of these advances provides a framework for the described classification of sexual precocity and delayed puberty.1 GnRH is synonymous with LHRH.

Animals↗
PubMed2005

Testosterone selectively reduces the high molecular weight form of adiponectin by inhibiting its secretion from adipocytes.

The antidiabetic hormone adiponectin circulates in blood as several oligomeric complexes, and the ratios between them are critical in determining insulin sensitivity. In this study we investigated the role of testosterone in regulating the oligomeric complex distribution of adiponectin. Gel filtration analysis revealed that circulating adiponectin existed as the forms of high molecular weight (HMW), middle molecular weight, and low molecular weight complexes in both human and mice. The concentration of HMW adiponectin in female was significantly higher than that in male, whereas there were no gender differences for the other two forms. Castration induced a dramatic elevation of the HMW form but had no effect on either the middle molecular weight or the low molecular weight form in mice. Testosterone treatment, on the other hand, caused a specific reduction of HMW adiponectin in the circulation. Pulse-chase labeling experiments in rat adipocytes revealed that the three oligomeric forms of adiponectin were secreted into the culture medium at different rates and that testosterone selectively impeded the secretion of HMW adiponectin but not the other two forms. The inhibitory effect of testosterone on secretion of HMW adiponectin was largely restored by the transcription inhibitor actinomycin D, suggesting the involvement of a transcriptional event in this process. The selective inhibition of HMW adiponectin by testosterone might contribute to the sex dimorphism of adiponectin in terms of its oligomeric complex distribution and could partly explain why men have higher risk to insulin resistance and atherosclerosis than women.

Adipocytes↗
PubMed1990

Time-courses of the appearance/disappearance of nuclear androgen + receptor complexes in the brain and adenohypophysis following testosterone administration/withdrawal to castrated male rats: relationships with gonadotropin secretion.

We characterized the temporal dynamics of brain and pituitary cell nuclear androgen receptor binding and serum androgen and gonadotropin levels associated with the implantation and removal of testosterone (T)-filled Silastic capsules into performed s.c. flank pouches of castrated, awake male rats. These capsules produced serum T levels in the physiologic range. The number of cell nuclear androgen + receptor complexes, as measured in an exchange assay using [3H]R1881, increased 15-fold at 0.5 h after capsule insertion in the HPAS (combined hypothalamus, preoptic area, amygdala and septum) and anterior pituitary gland, but then showed a second progressive rise within the next 8 h. This pattern suggests that T exerts an initial action in the tissues to alter the affinity and/or number of available androgen receptors. There was a lag time of 2-4 h to the first indication of negative feedback suppression of LH secretion. Serum LH levels declined only slightly at 4 h after capsule insertion but continued to fall thereafter, reaching undetectable values by 24 h. In contrast, serum FSH levels declined only slightly after 24 h of T exposure. After removal of the T capsules, serum T levels declined to castrate values within 2 h at which time the level of androgen + receptor complexes had fallen to 60% in the brain and pituitary. Serum LH and FSH concentrations were unchanged at 2 h after capsule removal, but rose significantly within the next 2 h. The data indicate that the occupation of androgen receptors rapidly changes in response to variations in circulating T in a fashion that implicates their involvement in the expression of this steroid's negative feedback actions on gonadotropin secretion.

Androgens↗
PubMed1981

Gonadotropin-releasing hormone analog and testosterone synergistically inhibit spermatogenesis.

We recently demonstrated that superactive gonadotropin-releasing hormone (GnRH) analogs and testosterone synergistically suppress gonadotropin secretion in castrate rats. We proposed that these two classes of agents used in combination would lead to enhanced suppression of spermatogenesis by synergistically inhibiting gonadotropin secretion. This hypothesis was tested in the present study in which synergistic inhibition of spermatogenesis was produced by combined analog and testosterone treatment. The mechanism of the synergistic action observed differed from that hypothesized in that the analog had both primary inhibitory actions directly on the testis and effects at a pituitary level. The addition of testosterone to the regimen further inhibited spermatogenesis by decreasing the secretion of gonadotropins thereby attenuating the compensatory rise in LH and FSH secretion expected with direct analog inhibition of the testis. These studies demonstrate the potential of combined GnRH analog and testosterone administration as a male contraceptive agent and indicate the complexity of their synergistic interactions.

Animals↗
PubMed1976

Endogenous anabolic agents in farm animals.

This presentation is limited to the three groups of steroid sex hormones which alone or in combination have been shown to be anabolic when used in farm animals. It seems essential for realistic evaluation of public health aspects of use of these hormones that the discussions include naturally occurring levels of the hormones. The following topics will be dealt with for each group of hormones: 1. Types and sources; 2. Production rates; 3. Plasma levels; 4. Tissue concentrations; 5. Metabolism and excretion. Gestagens. Progesterone and 20-dihydroprogesterones are mainly produced in ovaries and placenta. Production rates are estimated to 10 and 14 mg/24 hrs in pregnant goats and sheep, respectively. Plasma levels during the luteal phase are of the order of 2--10 ng/ml, during pregnancy somewhat higher. Muscular tissue from calves contain 0.25 mg/g. In dairy cows progesterone is excreted with the milk which contains up to 30 ng/ml; butterfat up to 300 mg/g. In ruminants progesterone is metabolized mainly to androgens excreted with faeces. In pigs large parts are metabolized to pregnanediols excreted with urine. Androgens. Testosterone is mainly secreted by testes. Boar testes also produce large amounts of dehydroepiandrosterone and its sulphate. Production rates have been estimated to be 10 mg and 40--50 mg/24 hrs. in boars and bulls respectively. Plasma levels in bulls and rams are generally 2--10 ng/ml, in boars 2--25 ng/ml. Adipose tissue levels up to 22 ng/g are reported for bulls. In ruminants epitestosterone seems to be a major metabolite excreted mainly with faeces. In boars, urinary 11-deoxy-17-ketosteroids are major metabolites of testicular dehydroepiandrosterone. Castration shows elimination to be rapid. Estrogens. 17beta-Estradiol and estrone are produced in ovaries and placenta and, in large amounts, in boar and stallion testes. Production rates in late pregnancy are estimated to 10 mg oestrone/24 hrs. in goats, 2 mg estrone and up to 28 mg 17beta-estradiol/24 hrs. in sheep. In cows much higher values are found. Boars and stallions produce huge amounts daily. Plasma levels in non-pregnant animals are at the pg/ml level. In late pregnancy levels of 2--4 thousand pg/ml are encountered in sows and cows, in sheep and goats lower levels. Calf muscular tissue contains up to 410 and 610 pg/g of estrone and 17beta-estradiol respectively. In muscle from pregnant heifers corresponding values were 120 and 860 pg/g in the 4th month and 2100 and 370 pg/g in the 9th month of pregnancy. Ruminants in large measure metabolize 17 beta-estradiol and estrone to 17alpha-estradiol which possesses low estrogenic activity. In pigs estrone dominates in blood and urine. Major routes of elimination arre with faeces in ruminants, with urine in pigs and horses. Elimination rates are high. Results obtained during the last few years clearly show that all three groups of steroid sex hormones occur in considerable concentrations in plasma and tissue...

Androstenedione↗
PubMed1998

Dual action of androgen on calcium signaling and luteinizing hormone secretion in pituitary gonadotrophs.

An increase in serum androgen levels associated with a suppression of cyclic gonadotropin secretion is frequently observed in females with impaired ovarian function. Here, we addressed the hypotheses that androgens (testosterone and dihydrotestosterone) alter gonadotropin secretion by modulating agonist-induced Ca2+ signaling and/or Ca(2+)-controlled exocytosis. In mixed populations of pituitary cells from female rats, addition of testosterone reduced basal and agonist (GnRH)-induced gonadotropin secretion in a concentration- and time-dependent manner. The suppressive actions of this androgen on gonadotropin secretion were observed over the full GnRH concentration range. Reduction in agonist-induced gonadotropin secretion was also observed after addition of dihydrotestosterone, indicating that the inhibitory action of testosterone is not mediated by its conversion to estradiol. Both the extracellular Ca(2+)-independent spike phase and extracellular Ca(2+)-dependent sustained phase of GnRH-induced gonadotropin secretions were affected by testosterone. In part, the inhibitory action of testosterone was mediated by attenuation of GnRH-induced InsP3 production and InsP3-dependent Ca2+ mobilization. In addition, testosterone exhibited a Ca(2+)-independent action on gonadotropin secretion, as documented by attenuation of high potassium-induced secretion without an affect on depolarization-induced Ca2+ signals. These results suggest that androgen inhibition of gonadotropin secretion occurs at two distinct steps in the secretory pathway, one prior to and one after elevation in cytosolic Ca2+ concentration.

Androgens↗
PubMed1994

Direct action of LH RH and its antagonist on isolated bovine granulosa cells steroidogenesis.

Progesterone, 4-androstene-3,17-dione, testosterone and estradiol-17 beta secretion by bovine granulosa cells culture without or in the presence of 10, 100 or 10.000 ng/ml LH RH or of its antagonist (D Phe2, D Phe6) LH RH were analyzed. It was observed that both LH RH and its antagonist significantly activated progesterone and estradiol output. LH RH also stimulated, but (D Phe2, D Phe6) LH RH inhibited granulosa 4-androstene-3,17-dione secretion. Both LH RH and its analogue decreased testosterone release by the cell culture. This is the first demonstration of a direct influence of LH RH on bovine ovarian steroidogenesis. The lack of correlation between LH RH and its agonist action on hypophysis and on different gonadal steroids secretion may suggest the differences in the features of receptors to LH RH-related peptides in the various target cells.

Androstenedione↗
PubMed1998

Recombinant human follicle-stimulating hormone administration increases testosterone production in men, possibly by a Sertoli cell-secreted nonsteroid factor.

We previously showed that recombinant human FSH (R-FSH) in males increased the testosterone (T) concentration in spermatic venous blood (SB). To investigate the effect of R-FSH on spermatic steroid levels and the action of steroid- and LH-free SB on isolated Leydig cells, nine normospermic males were studied during spermatic cord surgery. Peripheral blood and SB samples were collected before and 30 min after iv administration of 150 U R-FSH to measure LH, FSH, T, estradiol, 17alpha-hydroxyprogesterone, and sex hormone-binding globulin, and in SB, androstenedione (delta4) and dehydroepiandrosterone (DHEA) were also measured. LH bioactivity was assessed by in vitro production of T in isolated Leydig cells. The actions of R-FSH and SB (steroid and LH free) were analyzed in the bioassay. Data are expressed as the mean +/- SE. FSH in peripheral blood and SB increased by 411% and 477% after R-FSH administration. R-FSH induced a significant increase in spermatic T (basal vs. 30 min, 326.4 +/- 98.5 vs. 732.4 +/- 152.8 ng/mL; P < 0.047) and in spermatic estradiol (289.5 +/- 66.9 vs. 535.6 +/- 83.4 pg/mL; P < 0.036). The T/delta4 ratio (36.9 +/- 9.2 vs. 74.5 +/- 13.3; P < 0.019) and the T/DHEA ratio (10.8 +/- 1.1 vs. 22.4 +/- 4.9; P < 0.024) increased significantly. In isolated Leydig cells, R-FSH did not change T production, but the SB (steroid and LH free) after R-FSH administration induced an increase in T production (3.3 +/- 0.6 vs. 4.9 +/- 0.6 ng/tube; P < 0.04). LH-like activity was found in a more than 50,000-Da fraction after centrifugation in Amicon filters, even in the presence of anti-LH. These results suggest that R-FSH increases the production of T by Leydig cells through a Sertoli cell-released nonsteroid factor with a molecular mass greater than 50 kDa. The increase in the T/delta4 and T/DHEA ratios indicates that this factor would act by amplifying the LH response through the delta5 pathway and the 17beta-hydroxysteroid dehydrogenase enzyme.

Adult↗
PubMed1998

Behavioural and hormonal responses of the pied flycatcher to environmental stressors.

I investigated the effects of high plasma levels of corticosterone in male pied flycatchers, Ficedula hypoleuca, during the period of territorial establishment and the nestling period. In a second experiment males were exposed to a territorial intruder, a great spotted woodpecker model and a weasel model during the nest-building and nestling periods and their behavioural and hormonal reactions studied. Males were also exposed to handling stress (hormonal study) during these periods. During the period of territorial establishment, corticosterone-treated males, as well as control males, abandoned the territory in which they were captured; however, males in both groups very soon established new territories. During the nestling period, corticosterone-treated males, but not control males, abandoned their nests. During the nest-building period, intact males frequently attacked the territorial intruder but corticosterone-treated males never did; the woodpecker was only rarely attacked by intact males, and the weasel never. During the nestling period, the weasel was not attacked and territorial intruders only rarely; but woodpeckers were frequently attacked. With the progress of the breeding season, male flycatchers significantly reduced their sensitivity, in terms of the adrenocortical response, to all stressors tested. During the nest-building period, corticosterone levels were significantly higher in males exposed to handling, a weasel and a territorial intruder than in unmanipulated males; corticosterone levels in males exposed to a woodpecker did not differ from those in unmanipulated males; and testosterone levels were significantly elevated in males exposed to a woodpecker and to an intruder, but were reduced in males exposed to a weasel. Handling did not affect the testosterone level. During the nestling period, all groups showed low testosterone levels, and only exposure to a weasel and to handling increased corticosterone levels significantly. The results indicate that environmentally induced changes in testosterone and corticosterone secretion can be affected independently from one another, and that there are ecological bases for the differentiated hormonal responses to stress. Copyright 1998 The Association for the Study of Animal Behaviour. Copyright 1998 The Association for the Study of Animal Behaviour.

Journal Article↗
PubMed1984

Prostatic origin of fucosyl transferase in human seminal plasma--a study on healthy controls and on men with infertility or with prostatic cancer.

Fucosyl transferase was recovered in soluble form in human seminal plasma. The enzyme had very little activity, as it was structurally bound to prostasomes, which are membrane-surrounded organelles in seminal plasma. The fucosyl transferase activity was recorded on Sephadex G200 chromatography of seminal plasma (supernatant after ultracentrifugation) in one single peak coinciding with that of prostate-specific acid phosphatase. Studies on healthy men and on men with prostatic cancer suggest a prostatic origin of fucosyl transferase activity; two of the men with prostatic cancer displayed 50-95% decreased activities. Antiandrogenic therapy in another man with cancer resulted in substantial reductions in seminal plasma contents of fucosyl transferase, ATPase, acid phosphatase and fructose suggesting a role of testosterone in their secretions.

Acid Phosphatase↗
PubMed2006

Hormonal control of inhibin B in men.

Serum inhibin B (IB) and testosterone (T) levels, secreted by Sertoli cells (SC) and Leydig cells (LC), respectively, are parameters of the functional state of these cells. Whereas LC activity and, consequently, T secretion are regulated by serum LH, factors regulating IB secretion by SC are still partially unknown. There is evidence that under certain conditions such as puberty, aging or some spermatogenesis defects, LH levels or Gn-independent factors might contribute to regulating SC activity and IB secretion. Among these factors, GH and IGF-I as well as PRL might have a role. Therefore, in order to explore the possible effects of either LH alone and FSH alone or a combination of both Gn, respectively, on SC function, IB plasma levels and spermatogenesis, we studied their effects in 6 patients with hypogonadotropic hypogonadism (HH), whereas the effects of GH on these parameters were studied in 6 men with panhypopituitarism (PH). Finally, the possible effects of PRL on SC function and spermatogenesis were studied in 6 patients with hyperprolactinemia (HPRL); 24 normal, fertile adults served as control group. In men with HH, neither human chorionic Gn (hCG) nor FSH, respectively, were able to increase serum IB after 3 months of therapy, whereas combined Gn therapy for 24 months increased IB plasma levels and stimulated spermatogenesis in 4 out of 6 hypogonadal men. In panhypopituitaric men, GH added to the classical Gn therapy did not have an additional effect on serum IB levels or spermatogenesis. Surprisingly, in our hyperprolactemic men, IB plasma levels were increased and positively correlated (p<0.01) with serum PRL levels, whereas normalization of the latter by cabergoline treatment caused a decrease of IB levels and a moderate increase in T, LH and FSH. In conclusion, the lack of SC response to FSH therapy alone, as opposed to the response to combined Gn therapy, might indicate that normalization of serum T by hCG is required to obtain IB secretion by SC. Addition of GH did not affect SC function, serum IB levels or spermatogenesis. Finally, our data suggest that PRL plasma levels might have a direct role on IB secretion, suggesting that the hypogonadism found in patients with HPRL might be a consequence of both central (inhibition of Gn secretion) and peripheral (stimulation of IB secretion) origin.

Adult↗
PubMed1975

Neonatal hormone experience and adult lordosis and fighting in the golden hamster.

Androgenization by testicular secretions or exogenous testosterone propionate (TP treatments administered 24-48 hr post partum) suppressed sexual receptivity in the golden hamster. In response to prolonged adult estradiol benzoate (EB) treatment, gonadectomized normal females and neonatally castrated males exhibited significantly longer total lordosis durations than normal male or neonatally TP-treated (20 mug or 200 mug) females. These results suggest that one aspect of androgen-induced masculinization in the hamster involves reduced estrogen sensitivity. Responses to sequential EB followed by progesterone treatment were also lower in the androgenized groups. Neonatally castrated males did not differ significantly from normal females in their lordosis behavior. Irrespective of adult hormone treatment, androgenized animals fought more than normal females or neonatally castrated males. A genital mask was used to reduce sex differences in peripheral stimulation during testing.

Age Factors↗

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