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PubMed1982

Neutralization of gonadotropin-releasing hormone in neonatal rats with permanent impairment of the hypothalamic-pituitary-testicular axis.

Males rats were passively immunized at 5 days of age with a single 0.25 ml i.p. injection of gonadotropin-releasing hormone (GnRH) antiserum. Control animals were given an equal volume of normal rabbit serum (NRS). Serial blood determinations of gonadotropins, testosterone and dihydrotestosterone (DHT) were obtained at intervals ranging from early in life through adult life. Gonadotropin secretion was reduced (P less than 0.025) up to 35 days of age. Androgen secretion (testosterone) was reduced (P less than 0.05) at 10 and 33 days of age. When hCG was given to 54-day-old (young adult), and 100-day-old and 15-month-old animals, testosterone concentrations were similar in both experimental and control groups 1 h after hCG stimulation. As adults, basal gonadotropins were the same in both groups; however, after GnRH stimulation, the GnRH antiserum-treated groups showed an increased gonadotropin response when compared to the NRS control group. In order to determine whether there was an alteration in steroid feedback, other animals were castrated at adult age (approximately 100 days old), and exogenous testosterone was given in increasing increments. However, serum gonadotropins decreased similarly in treated and control groups. These data indicate that a single injection of GnRH antiserum early in life decreased gonadotropin secretion temporarily during prepubertal sexual development and caused a permanent alteration in hypothalamic-pituitary-testicular function.

Animals↗
PubMed1984

Steroid secretion by the human egg-corona-cumulus complex in culture.

Forty-five oocyte-corona-cumulus complexes ( OCCC ) were obtained from follicles of 13 women undergoing fertilization in vitro. Follicular growth was induced with human menopausal gonadotropin, and follicular aspiration was performed 36 h after an ovulatory injection of hCG. The maturation of these complexes was evaluated by the extent of cumulus mucification and corona cell dispersal. Three main morphological types were characterized: immature OCCCs (6), with a tight and compact corona-cumulus mass surrounding the oocyte; intermediate OCCCs (26), with a dispersed cumulus but only partly dispersed corona layer; and mature complexes (13) with complete dispersal of both cellular components. During a 24-h culture, progesterone secretion by intermediate and mature OCCCs was 30-fold higher (mean +/- SEM, 652 +/- 87 ng/ OCCC X 24 h) than immature OCCCs (19.6 +/- 3.5 ng/ OCCC X 24 h), while estradiol secretion was twice as high (3.8 +/- 1.1 vs. 1.2 +/- 0.6 ng/ OCCC X 24 h). Testosterone secretion was similar in all three types of OCCCs cultured (0.30 ng/24 h). It is suggested that the steroids produced by the OCCC may contribute to the local milieu of the fallopian tube.

Adult↗
PubMed1975

Changes in gonadotropin secretion following complete or hemicastration in the adult rat.

The effect of sham castration, hemicastration or complete castration on gonadotropin and testosterone secretion was studied in adult male rats. Untreated control rats were autopsied 1, 10, 20, 30 and 40 days following assignment to treatment groups. Sham-castrated controls were autopsied 1, 2 and 3 days after surgery. Complete and hemicastrates were autopsied 1, 2, 3, 10, 20, 30 and 40 days after surgery. Serum levels of both FSH and LH were elevated by 24 h postcastration and the levels of both gonadotropins continued to rise throughout the course of the experiment. Serum levels of LH rose following hemicastration and remained above control values through day 30. Serum FSH levels were not significantly affected by hemicastration. Compensatory testicular hypertrophy was not observed in hemicastrated rats.

Animals↗
PubMed2003

Sexual differentiation.

In humans, like as in other mammals, the gonads, the internal genital ducts, and the external genital structures all develop from bipotential embryologic tissues. Male or female phenotype develops through a cascade of processes which initiate with sex determination and follow with sex differentiation. The karyotype (46, XY or 46, XX) of the embryo (genetic sex) determines whether primordial gonad differentiates into a testis or an ovary, respectively (gonadal differentiation). A Y-related gene, SRY, acts as a switch signal for testis differentiation. Testis development process involves several steps controlled by other non-OY-linked genes, such as Wilms tumor gene 1 (WT1), EMX2, LIM1, steroidogenic factor 1(SF-1), SRY box-related gene 9 (SOX9). Since other genes, such as Wnt-4 and DAX-1, are necessary for the initiation of female pathway in sex determination, female development cannot be considered a default process. Hormonal production of differentiated gonads is relevant for differentiation of the internal and external genitalia during fetal life, and for the development of secondary sex characteristics at puberty. Antimullerian hormone (AMH) secreted by Sertoli cells inhibits the development of female internal genitalia (tube, uterus, upper part of vagina); testosterone secreted by Leydig cells induces stabilization of wolffian ducts and development of internal male genitalia. Differentiation of external male genitalia requires the transformation of testosterone to dihydrotestosterone by 5alpha reductase type 2 expressed in genital skin and urogenital sinus. The effects of androgens occur in presence of functional androgen receptor (AR) protein. Mutations of genes coding for steroidogenic enzymes, AMH, AMH receptor, AR and 5alpha reductase are all associated with impairment of sex differentiation and result in genital ambiguity.

Embryonic and Fetal Development↗
PubMed1986

Treatment of prostatic cancer with a depot form of a luteinizing hormone-releasing hormone analogue.

Chronic administration of a depot form of D-Trp6 luteinizing hormone-releasing hormone (LH-RH), an LH-RH analogue (3 mg i.m. every 28 days for a mean period of 9.1 months), to 14 patients with locally extended or metastatic cancer of the prostate provided a good degree of disease control. After a slight and transient increase in gonadotropin secretion, the peptide induced a sharp and long-lasting inhibition of both gonadotropin and testosterone secretion, contemporaneously with clinical improvement and without any important side effects. These results are comparable to those recorded by others after daily administration of LH-RH analogues.

Acid Phosphatase↗
PubMed1988

Effects of local heating of the testes on the concentration of testosterone in jugular and testicular venous blood of rats and on testosterone production in vitro.

Heating both testes of rats to between 39 degrees C and 41 degrees C for 30 min was apparently without effect 21 days later, but heating to between 41.5 degrees C and 43 degrees C for 30 min resulted in a significant drop in testis weight accompanied by significant rises in the serum levels of LH and FSH. There were no changes in serum testosterone concentration in the peripheral circulation although there were increases in the concentration in testicular venous blood. The ability of the heated testis to secrete testosterone in vivo in response to maximal stimulation by hCG was reduced, as judged by testosterone levels in peripheral blood, while there was a supranormal increase in testosterone levels in testicular venous blood. Maximally stimulated testosterone production in vitro by the heated testis was supranormal whereas the basal production of testosterone per testis was not different from control values. Therefore, it appears that the testosterone produced by Leydig cells from heated testes may not be secreted as effectively as in normal testes.

Animals↗
PubMed1981

Sertoli-Leydig cell communication via an LHRH-like factor.

The primary function of the testosterone secreted by Leydig cells is the maintenance of spermatogenesis and hence fertility. This action of testosterone is mediated by the Sertoli cells which nourish and support the developing spermatozoa. As normal Sertoli cell function is so critically dependent on normal Leydig cell function, a regulatory influence of the Sertoli cells on the Leydig cells has been suggested. Indeed, follicle-stimulating hormone (FSH), which acts only on Sertoli cells, can also cause profound changes in Leydig cell function, although how this is effected is unknown. We recently hypothesized that the Sertoli cell might be the source of a luteinizing hormone releasing hormone (LHRH)-like factor which we detected in the interstitial fluid surrounding the Leydig cells. As injected LHRH agonists cause impairment of gonadal function and directly inhibit FSH-induced changes in Leydig cell function through specific membrane receptors, this 'LHRH-like' factor has all the correct credentials for the postulated messenger between the Sertoli and Leydig cells. Here, we strengthen this case by demonstrating that seminiferous tubules from both the rat and the stumptailed macaque (Macaca arctoides) contain a factor which has LHRH-like receptor-binding and biological activity in vitro, but which is immunologically distinct from native LHRH. We have also shown that this factor is secreted in vitro by cultured rat Sertoli cells.

Animals↗
PubMed2000

New clinical applications of transdermal testosterone delivery in men and women.

This paper reviews recent progress in the development and clinical application of testosterone transdermal delivery systems designed for physiological replacement therapy in men and women. The biopharmaceutic goal of physiologic replacement therapy is to produce serum levels and circadian patterns of testosterone and its active metabolites that mimic the normal physiology of testosterone in the particular target population. For the treatment of adult hypogonadal men, the nightly 24 h application of the Androderm testosterone transdermal system (5 mg per day) achieves this goal - as demonstrated in a series of clinical pharmacokinetic studies. For the treatment of adolescent males, physiologic replacement can be approximated by modifying the dose and duration of Androderm application so as to mimic the patterns of nocturnal testosterone secretion observed during puberty. With the objective of providing physiological replacement for women with diminished testosterone production, an experimental testosterone matrix transdermal system (TMTDS) has been developed and is currently undergoing clinical evaluation. In parallel with the development of testosterone transdermal systems, physicians have been investigating a number of conditions, in both males and females, where testosterone production is diminished and replacement therapy may be beneficial. Three of these new clinical applications will be illustrated - the use of Androderm for the treatment of adolescent males with beta-thalassemia, the use of Androderm for the treatment of HIV+ men, and the use of the TMTDS for the treatment of HIV+ women. From the biopharmaceutic and clinical perspectives, the development of testosterone transdermal systems represents an important achievement in controlled drug delivery.

Administration, Cutaneous↗
PubMed1976

Effect of alcohol (ethanol) administration on sex-hormone metabolism in normal men.

To determine whether ethanol per se affects testosterone metabolism, alcohol was administered to normal male volunteers for periods up to four weeks, resulting in an initial dampening of the episodic bursts of testosterone secretion followed by decreases in both the mean plasma concentration and the production rate of testosterone. The volunteers received adequate nutrition and none lost weight during the study, which tended to exclude a nutritional disturbance as the cause of the decreased testosterone levels. The changes in plasma luteinizing hormone suggested both a central (hypothalamus-pituitary) and gonadal effect of alcohol. In addition, alcohol consumption increased the metabolic clearance rate of testosterone in most subjects studied, probably owing to the combined effects of a decreased plasma binding capacity for the androgen and increased hepatic testosterone A-ring reductase activity. These results indicate that alcohol markedly affects testosterone metabolism independently of cirrhosis or nutritional factors.

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗
PubMed1980

Morphometric analysis of Leydig cells in the normal rat testis.

Leydig cells are thought to be the source of most, if not all, the testosterone produced by the testis. The goal of this study was to obtain quantitative information about rat Leydig cells and their organelles that might be correlated with pertinent physiological and biochemical data available either now or in the future. Morphometric analysis of Leydig cells in mature normal rats was carried out on tissue fixed by perfusion with buffered glutaraldehyde, and embedded in glycol methacrylate for light microscopy and in Epon for electron microscopy. In a whole testis, 82.4% of the volume was occupied by seminiferous tubules, 15.7% by the interstitial tissue, and 1.9% by the capsule. Leydig cells constituted 2.7% of testicular volume. Each cubic centimeter (contained approximatelyy 1 g) of rat testis contained about 22 million Leydig cells. An average Leydig cell had a volume of 1,210 micron3 and its plasma membrane had a surface area of 1,520 micron2. The smooth endoplasmic reticulum (SER), the most prominent organelle in Leydig cells and a major site of steroidogenic enzymes, had a surface area of approximately 10,500 micron2/cell, which is 6.9 times that of the plasma membrane and is 60% of the total membrane area of the cell. The total surface area of Leydig SER per cubic centimeter of testis tissue is approximately 2,300 cm2 or 0.23 m2. There were 3.0 mg of Leydig mitochondria in 1 g of testis tissue. The average Leydig cell contained approximately 622 mitochondria, measuring on the average 0.35 micron in diameter and 2.40 micron in length. The mitochondrial inner membrane (including cristae), another important site of steroidogenic enzymes, had a surface area of 2,920 micron2/cell, which is 1.9 times that of the plasma membrane. There were 644 cm2 of inner mitochondrial membrane/cm3 of testis tissue. These morphometric results can be correlated with published data on the rate of testosterone secretion to show that an average Leydig cell secretes approximately 0.44 pg of testosterone/d or 10,600 molecules of testosterone/s. The rate of testosterone production by each square centimeter of SER is 4.2 ng/d or 101 million molecules/s: the corresponding rate for each square centimeter of mitochondrial inner membrane is 15 ng testosterone/d or 362 million molecules/s.

Animals↗
PubMedDate not supplied

Brain-periphery connections: do they play a role in mediating the effect of centrally injected interleukin-1 beta on gonadal function?

The immune system and several endocrine axes communicate with each other through a network of molecules which collectively produce a coordinated response to immune challenges. This phenomenon, necessary for the survival of the organism, is thought to involve the release, by activated cells in the periphery, of proteins, called cytokines, which inform the brain about immune activation. The brain then organizes a series of neuroendocrine responses which participate in the regulation of the host response. With regard to the influence of cytokines on the hypothalamic-pituitary-gonadal axis, we know that the injection of these proteins lowers gonadotropin-releasing hormone release, which in turn inhibits luteinizing hormone (LH) secretion. These changes would be expected to decrease sex steroid production and, indeed, estrogens and testosterone are low in female and male rats, respectively, following acute intracerebroventricular (i.c.v.) injection of interleukin (IL)-1 beta. There is, however, another possibility that central cytokines could alter ovarian and testicular function independently of changes in gonadotropin levels. Prolonged i.c.v. infusion of the cytokine into the female rat brain produced a dramatic rise in progesterone levels. The absence of a comparable change in the progesterone release rate of males infused with IL-1 beta, and the presence of marked surges of prolactin (PRL) in the females, suggests that IL-1 beta altered ovarian function, and that the persistence of large corpora lutea induced PRL release. The possibility that the cytokine might stimulate the brain circuits that regulate PRL release, while possible, appears remote, because male rats injected with IL-1 beta showed significantly blunted PRL levels. In intact adult male rats, i.c.v. IL-1 beta administration caused the expected decrease in LH and testosterone levels, but was also accompanied by a loss of testicular responsiveness to gonadotropins. Though elevated levels of corticosteroids are known to interfere with normal gonadal steroidogenesis, blockade of IL-1-induced corticosterone release did not reverse the inhibitory influence of the cytokine. One mechanism that deserves attention is the possibility that i.c.v. injection of IL-1 beta might increase circulating cytokine levels, and indeed plasma IL-6 concentrations were significantly elevated in rats treated with IL-1 beta. This humoral mechanism may disrupt testicular function through the documented inhibitory effects of blood-borne cytokines on Leydig cell function. In addition, brain cytokines might influence a variety of peripheral events through direct (neural?) connections. This brief review discusses the hypothesis that there are brain-to-gonad connections that bypass the pituitary, and presents results that might support the possibility that central injection of IL-1 beta decreases testosterone secretion independently of blunted LH levels.

Animals↗
PubMed2006

Analytical and physiological factors affecting the interpretation of serum testosterone concentration in men.

Most hospital laboratories estimate the concentration of total circulating testosterone using a non-extraction method on an automated multi-channel immunoassay analyser supplied by a small number of multi-national diagnostic companies. Although these platforms offer advantages of quick turnaround times, small volume sampling and random access analysis, proficiency testing schemes suggest the quality of results produced remains similar to that of the early manual radioimmunoassay. An estimate of the bioavailable, non-sex hormone binding globulin (SHBG) bound fraction of circulating testosterone, be that the free or the free plus albumin-bound, may be a better index of gonadal status than total testosterone alone, especially when a borderline hypogonadal level of total testosterone is found, and may avoid misclassification of hypogonadal or eugonadal men. Free or bioavailable testosterone may be calculated or measured. The free androgen index may not give a true reflection of androgen status in men. In the interpretation of serum testosterone concentrations with results >40 nmol/L, the possibility of exogenous administration or abuse needs to be considered. The marked diurnal rhythm in total testosterone should also be taken into account. There may be a diminution of testosterone secretion with advancing age, but the great majority of older men have a circulating total testosterone concentration well within the accepted reference intervals established for younger men. As testosterone concentration may fluctuate markedly both seasonally and from day to day, it may be judicious to measure levels on more than one occasion. Provided that estimates of serum testosterone are unequivocally eugonadal (12.5-40 nmol/L) or hypogonadal (<7.0 nmol/L), results produced by routine automated immunoassays will in all probability give a satisfactory assessment of androgen status in men.Routine biochemical assessment of gonadal function in men should include measurement of early morning luteinizing hormone, follicle stimulating hormone, prolactin and SHBG together with total testosterone, and if necessary some estimate of bioactive testosterone.

Aging↗
PubMed2006

Anti-Müllerian hormone in disorders of sex determination and differentiation.

Masculinisation of internal and external genitalia during foetal development depends on the existence of two discrete testicular hormones: Leydig cell-secreted testosterone drives the differentiation of the Wolffian ducts, the urogenital sinus and the external genitalia, whereas Sertoli cell-produced anti-Müllerian hormone (AMH) provokes the regression of Müllerian ducts. The absence of AMH action in early foetal life results in the formation of the Fallopian tubes, the uterus and the upper third of the vagina. In 46,XY foetuses, lack of AMH may result from testicular dysgenesis affecting both Leydig and Sertoli cell populations: in this case persistence of Müllerian remnants is associated with ambiguous or female external genitalia. Alternatively, defective AMH action may result from mutations of the genes encoding for AMH or its receptor: in this condition known as Persistent Müllerian Duct Syndrome, testosterone production is normal and external genitalia are normally virilised. Finally, AMH may be normally secreted in intersex patients with defects restricted to androgen synthesis or action, resulting in patients with female or ambiguous external genitalia with no Müllerian derivatives.

Anti-Mullerian Hormone↗
PubMed1979

Plasma testosterone levels in intact and hemicastrated growing cockerels.

Changes in the levels of testosterone in plasma were measured by radioimmunoassay in blood samples taken at frequent intervals between 2 and 26 weeks of age from entire cockerels and cockerels hemicastrated before 2 weeks of age. In both groups the pattern of testosterone secretion could be divided into three clearly defined phases. In young birds, the levels of testosterone in plasma were low (0.3 ng/ml) but in the prepubertal period, at 11 weeks of age, they started to rise and continued to rise until 22 weeks of age when adult levels, which fluctuated between 2.5 and 3.5 ng/ml, were reached. In the immediate period after hemicastration, the concentration of testosterone decreased temporarily. From 11 weeks of age the levels of testosterone in the hemicastrated birds were approximately 75% of those in intact birds. These results are discussed in relation to the compensatory testicular hypertrophy which occurs in growing cockerels hemicastrated at an early age.

Animals↗
PubMed1989

Serum and testicular testosterone and androgen binding protein profiles following subchronic treatment with carbendazim.

While the general toxicity of the benzimidazole pesticides for mammals is low, one of these compounds, carbendazim (MBC), causes degeneration of testicular tissue and decreases spermatogenic activity at doses well below the LD50 value. A study conducted by S. D. Carter, R. A. Hess, and J. W. Laskey (1987, Biol. Reprod. 37, 709-717) showed that treatment with 400 mg/kg/day MBC resulted in severe seminiferous tubular atrophy and infertility. Since spermatogenesis is an androgen-dependent process, we characterized the effects of MBC (0-400 mg/kg/day) on the endocrine function of the rat testes. Following subchronic (85 day) exposure, serum hormones (TSH, LH, FSH, and Prl) were measured as were androgen binding protein (ABP) and testosterone in testicular fluids (interstitial fluid and seminiferous tubule fluid). In addition, the functional capacity of the Leydig cell to secrete testosterone was assessed in vitro following an hCG challenge. Subchronic treatment with MBC at doses of 50-100 mg/kg/day had no effect on pituitary or testicular hormone concentrations: 200 mg/kg/day elevated the testosterone concentration in the seminiferous tubule fluid and the ABP concentration in both the interstitial fluid and the seminiferous tubule fluid without affecting serum testosterone or ABP concentrations. The 400 mg/kg/day dose resulted in increased concentration of both testosterone and ABP in the interstitial fluid and seminiferous tubule fluid and elevated serum ABP, with no change in serum testosterone. This endocrine profile is consistent with the testicular atrophy and "Sertoli cell-only" syndrome seen in these animals as reported by Gray et al. (1987, Toxicologist 7, 717). We conclude that seminiferous tubule fluid testosterone may be a result of two factors: (1) increased interstitial fluid testosterone concentrations and (2) decreased testosterone outflow from the testis to the general circulation. Also, increased ABP in the interstitial fluid may reflect a change in the relative secretion of ABP into the interstitial fluid and the seminiferous tubules.

Androgen-Binding Protein↗
PubMed1982

Menopausal endocrinology and management.

Entry into menopause is associated with a severe diminution of ovarian estrogen and progesterone secretion and a reduction of circulating androgens, although, in the presence of ovaries, a degree of testosterone secretion persists. Menopause is associated to a varying degree and severity, with hot flashes--a disorder of central thermoregulation--progressive sex tissue atrophy, and accelerated bone mineral loss that eventually leads to a substantial prevalence of osteoporosis, with spine, hip, and radial fractures, particularly in thin, inactive smokers with low calcium intake. Treatment with estrogens eliminates hot flashes and sex tissue atrophy and prevents osteoporosis. Unfortunately, oral estrogen therapy results in overstimulation of the liver, producing secreted proteins and an increased risk of endometrial carcinoma and gallbladder disease. The addition of a progestogen will diminish the risk of endometrial carcinoma, presumably by reducing estrogen-receptor concentration and increasing estradiol dehydrogenase activity but will usually result in vaginal bleeding in women with uteri. The use of estrogen therapy with or without a progestin should be an informed joint decision of physician and patient that must be reevaluated regularly as new information becomes available.

Adult↗
PubMed1997

Ecological constraints and the evolution of hormone-behavior interrelationships.

Vertebrates show a diverse array of social behaviors. Equally complex are the mechanisms by which these behavioral patterns are regulated by hormones and the effects of behavioral interactions on hormone secretion. Nonetheless, comparative field and laboratory experiments indicate that general underlying themes, including mechanisms, may exist. For example, comparative studies in birds reveal that testosterone activates a type of aggression, territorial behavior, in those species that are territorial only during the breeding season. Territoriality at other times appears to be independent of sex steroid control, although qualitatively and quantitatively the behavior appears identical. Similarly, formation of pair bonds appears to be complex. In some populations such bonds are sexual, whereas in others they appear to be alliances possibly for joint defense of a territory. In cooperative groups of birds, pair bonds and alliances may exist simultaneously. Testosterone appears to be important for activation of the courtship behavior that leads to formations to sexual pair bonds. However, many investigations indicate that pair bonds in nonsexual contexts are not regulated by testosterone. Hormonal mechanisms underlying the establishment of alliances (if any) remain unknown. Clearly, these complex behavioral patterns due to seasonal changes and variation in context pose important questions for control mechanisms. One obvious question is, why this diversity in control mechanisms? It appears that there are evolutionary "costs" to high circulating levels of testosterone. They can be energetic costs or may involve increased predation risk or reduced survival after wounding. In males that express parental behavior, high circulating testosterone levels interfere with parental care, resulting in reduced reproductive success. Thus, regulation of testosterone secretion must balance the need to compete with other males as well as provide parental care. High circulating levels of testosterone for prolonged periods are also known to suppress the immune system. This latter effect may have profound implications for the development of androgen-dependent secondary sex characteristics that have evolved through sexual selection. There are several ways to avoid potential "costs" of hormone secretion at inappropriate times. A hormone may be metabolized at its target cell to another form that then binds to a different receptor (e.g., aromatization of testosterone to estradiol). Also receptors may be downregulated in tissues that would otherwise respond inappropriately in a specific life history state. On the other hand, multiple hormone mechanisms may have evolved to activate behavioral traits at the right time and in the correct context. When a behavioral trait is expressed throughout the life cycle, hormones may potentially deactivate behavior for short periods. With detailed investigations of organisms in their natural environment we can determine the potential ecological costs underlying hormone-behavior interactions that, in turn, shed light on their evolution. These data also indicate a number of problems for hormonal control mechanisms, but also indicate trends, alternatives, and hopefully in the future a more complete understanding of common mechanisms underlying behavioral endocrinology at the cell and molecular level. Only then will we be able to predict when and where specific mechanisms of hormone-behavior interactions operate and how they evolved.

Animals↗
PubMed2001

Cortisol affects testicular development in male common carp, Cyprinus carpio L., but not via an effect on LH secretion.

Previous work showed that prolonged elevated cortisol levels, implicated in the stress adaptation, inhibits testicular pubertal development in male common carp, as well as an impairment of the synthesis of the 11-oxygenated androgens. This may be a direct effect of cortisol on the testis or via the gonadotropin secretion by the pituitary. The aim of the present study was to investigate whether cortisol has an effect on pituitary LH secretion. Juvenile common carp were fed with cortisol containing food pellets. Elevated cortisol levels blocked the increase in testosterone levels and pituitary LH content, but induced higher plasma LH levels at the end of puberty. The in vitro LH release capacity was correlated to the pituitary LH content. At the final stage of pubertal development, when a significant difference in pituitary LH content was observed, sGnRHa-induced LH release was also decreased. Testosterone has been shown to induce development of pituitary gonadotrophs, leading to an increase in LH content and GnRH-inducible LH release, but a decrease in plasma LH levels. We observed decreased plasma testosterone levels as a consequence of prolonged cortisol treatment. It is hypothesised that cortisol inhibits the testicular testosterone secretion and thereby, prevents LH storage. In vitro, this leads to a reduced GnRH-inducible LH release, but in vivo to increased LH plasma levels. It is very unlikely that the impaired testicular development is due to an effect of cortisol on LH secretion.

Animals↗