[Effects of testosterone and LH-RH on oxytocin secretion (author's transl)].
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Increased LH and FSH secretion after cranial irradiation in boys.
The effect of high-dose cranial- and craniospinal irradiation and chemotherapy on the gonadotropin-sex steroid axis was studied during different stages of puberty by measuring pulsatile secretion of luteinizing hormone (LH), follicle-stimulating hormone (FSH) and testosterone. The patients were thirteen boys who had been treated for malignant brain tumor residing well away from the hypothalamo-pituitary region. The median time to follow-up was 9 (1-16) years. The onset of puberty was early in the patients, median 10.5 years, compared to the average age for Swedish boys, which is at median 12.4 years. There was, before puberty, no significant difference in LH and FSH secretion between patients and a control group of normal boys. In early, mid- and late stages of puberty, however, LH and FSH secretion was increased in the patients overall, whereas testosterone secretion was maintained within the normal range in spite of signs of gonadotoxocity with small testicular volumes. These results indicate that the vulnerable parts of the gonadotropin releasing hormone (GnRH)-gonadotropin (LH, FSH)-gonadal axis are the regulatory system that determines the timing of pubertal induction and the gonads. The GnRH-LH, FSH-releasing neurons appear relatively resistant to cranial irradiation as they are able to respond with supranormal LH and FSH levels for long periods of time after treatment.
Adolescent↗
Effect of testosterone and season on proenkephalin messenger RNA expression in the preoptic area of the hypothalamus in the ram.
Enkephalin appears to exert an inhibitory action on LH secretion, but whether testosterone regulates enkephalin gene expression is unknown. This study tested the hypothesis that testosterone and/or season modulate preproenkephalin mRNA expression in specific areas of the hypothalamus. Romney Marsh rams were castrated (wethers) either during the breeding season or nonbreeding season and received intramuscular injections of either oil or testosterone propionate (five/group). Blood samples were taken for the assay of plasma LH and testosterone. Preproenkephalin mRNA expression was quantified in hypothalamic sections by in situ hybridization. Mean plasma LH concentrations were reduced and the interpulse interval for LH pulses was greater in testosterone propionate-treated wethers compared with oil-treated wethers, with no change in LH pulse amplitude. Testosterone propionate treatment reduced proenkephalin expression in the diagonal band of Broca, the caudal preoptic area, and the bed nucleus of the stria terminalis. Seasonal differences in proenkephalin expression were observed in the bed nucleus of the stria terminalis, lateral septum, periventricular nucleus, and paraventricular nucleus. No differences were observed between treatments in seven other regions examined. We conclude that testosterone and season regulate proenkephalin mRNA levels in the preoptic area/hypothalamus in the ram in a region-specific manner.
Animals↗
Gonadal steroid modulation of LHRH-stimulated LH secretion by pituitary cell cultures.
Enzymatically dispersed rat pituitary cells were grown in primary culture, and LHRH-stimulated LH secretion was measured. Testosterone (T) decreased and 17 beta-estradiol (E) increased pituitary responsiveness to LHRH. The effect of E on LH secretion was partly due to an increase in LH content. There was a latent period of 12 h for E and 18 h for T between the onset of steroid treatment and the manifestation of steroid action. Neither steroid was required to be continuously present in order to exert its effects. After steroid withdrawal, the effect of T persisted for 72 h and that of E for more than 96 h. The actions of both steroids were blocked by protein-synthesis inhibitors. These results are consistent with the hypothesis that steroid effects rely on a mechanism involving alterations in protein synthesis; the affected proteins may be involved in the process of LHRH action.
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Decreases in the size and proliferation rate of VIP-immunoreactive cells induced in vitro by testosterone are associated with decreases in VIP release.
As in vitro study was carried out to determine whether testosterone directly inhibits the secretion of pituitary vasoactive intestinal peptide (VIP). A study was also conducted to elucidate the repercussions of treatment with 10(-6) M testosterone of monolayer cultures in the size and proliferation rate of pituitary VIP-immunoreactive cells, using double immunocytochemical labelling for proliferating cell nuclear antigen (PCNA) and VIP. Testosterone decreased the in vitro release of VIP from pituitary cells. It also decreased the percentage of pituitary VIP-immunoreactive and PCNA- and VIP-immunoreactive cells and decreased the size of the cellular and nuclear areas of these cells. Our results suggest that the inhibition of pituitary VIP secretion induced by testosterone could be exerted at pituitary level and that testosterone could act as a modulator of the proliferation rate of rat pituitary VIP-immunoreactive cells.
Animals↗
Relationship of serum leptin concentration with age, gender, and biomedical parameters in healthy, non-obese subjects.
It is known that the circulating levels of leptin, the adipocyte hormone implicated in the control of energy balance, are correlated with fat body mass (FBM), although the influences of other physiological conditions are not fully understood. We investigated the relationships of serum leptin concentration with age, gender, and 36 hormone-metabolic parameters in a sample of a well defined healthy population (n=246; age range 20-93 years), and in subgroups of lean individuals according to their body mass index (BMI), within similar age range and gender distribution. Only insulin secretion (positively) and testosteronemia (negatively, in males) show direct correlations. The other relationships are not significant but throughout collaborating variables, such as serum lipids, especially through FBM, lean body mass (LBM) through insulin secretion, and gender through FBM. In males, LBM correlates with insulin secretions, s-IGF-1 and with s-testosterone. The relationship between insulin secretion and LBM persists up to advanced age. From the present study it may be concluded that the positive relationship of leptin with insulin secretion and the negative one with testosterone, indicate direct implications of leptin in insulin signaling, as well as in male sexual development. Finally, the fact that the amount of secreted insulin depends on LBM and the latter on testosterone and IGF-1, indicates the importance of muscle mass in the control of insulin secretion.
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Hypokalemia decreases testosterone production in male mice by altering luteinizing hormone secretion.
Potassium deficiency produced by feeding mice a low potassium diet caused a marked decrease in plasma and testicular testosterone concentrations and a concomitant fall in the weight of seminal vesicles and in renal ornithine decarboxylase activity. All of these parameters were rapidly restored when potassium supply was normalized. Immunocytochemical analysis of gonadotropes and plasma LH values suggested that the pulsatile liberation of LH by the pituitary was impaired in the potassium-deficient male mice. Because the synthesis of testosterone in the potassium-deficient mice was stimulated by exogenous LH, hCG, or GnRH, one can conclude that alteration of the transcellular potassium gradient could affect the regulation of the hypothalamo-hypophyseal-testicular axis by affecting the pulsatile release of GnRH. Our results showing that the stimulation of LH secretion after castration was similar in control and potassium-deficient male mice suggest that a testicular factor(s) different from testosterone could be implicated in the abnormal regulation of LH secretion in potassium-deficient mice. We conclude that plasma potassium concentration is an important factor in the regulation of gonadotropin secretion and testicular functions.
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Proceedings: Effect of sex steroids on testosterone, oestradiol-17beta and luteinizing hormone secretion after the injection of synthetic luteinizing hormone releasing hormone into male dogs.
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Poly-A+ mRNA and defeminization of sexual behavior and gonadotropin secretion in rats.
To test the hypothesis that testosterone (T) sexually differentiates gonadotropin secretion and sexual behavior by inducing synthesis of messenger RNA (mRNA), newborn female rats received intrahypothalamic infusions of saline or cordycepin, an adenosine analogue that preferentially inhibits synthesis of polyadenylated mRNA, an hour before they received T propionate (TP) systemically. As adults, controls were anovulatory and did not become sexually receptive when given estradiol benzoate (EB) and progesterone (P). Cordycepin-treated females obtained lordosis quotients (LQs) three times those of controls and most of them ovulated. Cordycepin also curtailed the defeminizing effects of some doses of moxestrol, an artificial estrogen; thus it does not simply block aromatization. Some groups were retested for lordosis using EB and methysergide to bypass P receptors. Methysergide increased LQs in one group that received moxestrol + cordycepin as neonates and that was moderately responsive to P, but it did not increase sexual receptivity among the saline-treated controls. These data suggest that defeminization of sexual behaviour involves more than defeminization of P receptor synthesis.
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Evidence for decreased secretion of gonadotropin-releasing hormone in pubertal boys during short-term testosterone treatment.
Information about the site(s) of action as well as the age-dependent effects of sex steroids on gonadotropin-releasing hormone and gonadotropin secretion during human puberty is limited. To begin to address these questions, we evaluated the effects of a depot preparation of testosterone (testosterone enanthate) on gonadotropin secretion and pituitary responses to synthetic GnRH in 10, early to mid-pubertal boys who had either isolated GH deficiency (n-2) or delayed adolescent maturation (n-8). Chronological and bone age ranges were 13 1/12-16 1/12 and 11-14 yr, respectively. Frequent blood withdrawal studies (every 20 min for 20 consecutive h) were performed in the Clinical Research Center over two consecutive weekends. Following each study, gonadotropin responses to GnRH (0.25 microgram/kg iv bolus) were determined. During the initial study, all boys showed a sleep-entrained increase in luteinizing hormone (LH) and testosterone (T) secretion; mean nocturnal concentrations of LH and T were 2.3-fold greater than daytime values. At the end of the first study, testosterone enanthate was given im (0, 25, 50, or 75 mg/m2). Six days later, mean plasma T concentrations were in the pubertal to mid adult male range and were constant throughout the day: 25 mg/m2, 3.7 +/- 0.4 (SE) ng/ml; 50 mg/m2, 4.6 +/- 0.2 ng/ml; and 75 mg/m2, 6.7 +/- 0.4 ng/ml. T treatment had no effect on pituitary responses to GnRH: mean LH increment was 8.5 mIU/ml before and 10.0 mIU/ml after T treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
Adolescent↗
Analysis of bidirectional pattern synchrony of concentration-secretion pairs: implementation in the human testicular and adrenal axes.
The hypothalamo-pituitary-testicular and hypothalamo-pituitary-adrenal axes are prototypical coupled neuroendocrine systems. In the present study, we contrasted in vivo linkages within and between these two axes using methods without linearity assumptions. We examined 11 young (21-31 yr) and 8 older (62-74 yr) men who underwent frequent (every 2.5 min) blood sampling overnight for paired measurement of LH and testosterone and 35 adults (17 women and 18 men; 26-77 yr old) who underwent adrenocorticotropic hormone (ACTH) and cortisol measurements every 10 min for 24 h. To mirror physiological interactions, hormone secretion was first deconvolved from serial concentrations with a waveform-independent biexponential elimination model. Feedforward synchrony, feedback synchrony, and the difference in feedforward-feedback synchrony were quantified by the cross-approximate entropy (X-ApEn) statistic. These were applied in a forward (LH concentration template, examining pattern recurrence in testosterone secretion), reverse (testosterone concentration template, examining pattern recurrence in LH secretion), and differential (forward minus reverse) manner, respectively. Analogous concentration-secretion X-ApEn estimates were calculated from ACTH-cortisol pairs. X-ApEn, a scale- and model-independent measure of pattern reproducibility, disclosed 1) greater testosterone-LH feedback coordination than LH-testosterone feedforward synchrony in healthy men and significant and symmetric erosion of both feedforward and feedback linkages with aging; 2) more synchronous ACTH concentration-dependent feedforward than feedback drive of cortisol secretion, independent of gender and age; and 3) enhanced detection of bidirectional physiological regulation by in vivo pairwise concentration-secretion compared with concentration-concentration analyses. The linking of relevant biological input to output signals and vice versa should be useful in the dissection of the reciprocal control of neuroendocrine systems or even in the analysis of other nonendocrine networks.
Adult↗
Restoration of pulsatile luteinizing hormone secretion after fasting in rhesus monkeys (Macaca mulatta): dependence on size of the refeed meal.
In men and adult male rhesus monkeys brief periods of fasting (i.e. 1-2 days) can often lead to a suppression of hypothalamic-pituitary-testicular axis activity, marked by decreased circulating concentrations of LH, FSH, and testosterone. Refeeding a normal meal can rapidly restore normal secretory patterns of LH and testosterone. To learn more about the nature of the signal that links reproductive hormone secretion to nutrient intake, we examined whether the degree of restoration of pulsatile LH and testosterone secretion after a brief period of fasting is influenced by the size of the refeed meal. Adult male rhesus monkeys had indwelling venous catheters surgically implanted and were maintained on swivel/tether systems for remote collection of blood samples. Monkeys were fasted for 1 day and then on the following day they were refed one of five meals which varied in size and calorie content (i.e. 0 Cal/0 pellets Purina monkey chow; 100 Cal/5 pellets; 200 Cal/10 pellets; 300 Cal/15 pellets; or 600 Cal/30 pellets). Blood samples were collected from 0800-2400 h at 20-min intervals on the days of refeeding and assayed for LH and testosterone content. After a day of fasting, the frequency of pulsatile LH secretion the following morning was very low (0.56 +/- 0.1 pulses/3 h, measured from 0800-1100 h). When monkeys were not refed (i.e. were subjected to a second day of fasting; 0 pellet group) LH pulse frequency remained low [2.88 +/- 0.72 pulses/13 h, measured from 1100-2400 h (equivalent to 0.66 pulses/3 h)] throughout the day and evening hours. Refeeding monkeys 5, 10, 15, and 30 pellets caused a progressive stimulation of pulsatile LH secretion (3.17 +/- 0.54, 3.67 +/- 0.56, 5.5 +/- 0.67, and 6.38 +/- 0.53 pulses/13 h, respectively). Like LH pulse frequency, mean circulating LH and testosterone concentrations progressively increased as the size of the refeed meal was increased. For all three parameters (i.e. LH pulse frequency, mean LH concentration, and mean testosterone concentration) there was a significant, P less than or equal to 0.001, linear trend with increasing meal size. These findings indicate a very strong relation between the level of nutritional intake and the level of central drive to the reproductive axis during nutritional recovery from fasting, and suggest a physiological parameter that responds in a progressive fashion to increasing food intake serves as the signal to link central drive to the reproductive axis to changes in nutrient intake.(ABSTRACT TRUNCATED AT 400 WORDS)
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In vitro application of testosterone potentiates gonadotropin-releasing hormone-stimulated gonadotropin-II secretion from cultured goldfish pituitary cells.
The in vitro effects of overnight treatment with testosterone (T) on gonadotropin (GTH)-II secretion from primary cultures of dispersed female goldfish pituitary cells were examined. T (100 nM) did not affect basal GTH-II release, but increased GTH-II responses to initial applications of 0.5-h pulses of sGnRH or cGnRH-II in cells from females at sexually regressed, recrudescing, or mature (prespawning) stages. Pretreatment with 10 nM T was also effective, except in experiments with cells from sexually regressed females. Analysis of GTH-II response profiles to the first GnRH pulse revealed that T increased the size of the initial (first 15 min) and sustained (rest of response) release phases, and the duration of the total response to both GnRHs. These results indicate that direct positive influence of T on GnRH-stimulated GTH-II release is demonstrable in cells from female goldfish at all ovarian maturational stages; in addition, T affects both the initial and the sustained response phases. However, compared to the initial GnRH challenge, responses to a second 0.5-h GnRH pulse were decreased in T-treated but not in control cells, suggesting that T also enhanced desensitization. Ovarian maturational conditions modulated the effects of T on the GTH-II response kinetics. In cells prepared from sexually regressed females, T treatment changed the "monophasic" (initial phase only) GTH-II response to sGnRH to a "biphasic" one characteristic of cells prepared from fish at later stages of gonadal recrudescence. Advancing gonadal maturity increased the magnitude of both initial and sustained phases of the T-enhanced GTH-II response to sGnRH, but only elevated the initial phase of T-potentiated cGnRH-II-induced release. Direct actions of T on pituitary cells may play a role in ovarian steroid feedback regulation of GTH-II secretion during the seasonal reproductive cycle in goldfish.
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The influence of reproductive hormones on ANF release by rat atria.
The effects of subcutaneous (sc) administration of estradiol (50 micrograms/100 microliters/day x 10 day) or testosterone (15 mg/100 microliters twice a week x 2 weeks) on ANF release were examined in isolated perfused rat atria. The concentration of ANF in the perfusate was measured by radioimmunoassay, under basal conditions (atrial wall unstressed), and during atrial distention (intraluminal pressure raised to 4, 6, and 10 cm water). In both male and female control (vehicle-injected) groups, increased atrial pressure resulting in distention of the atrium caused a significant increase in ANF release. Estradiol increased basal secretion of ANF but did not influence stretch-induced stimulation of ANF secretion. By contrast, although testosterone did not affect basal secretion, it completely abolished the stretch-induced increase in ANF secretion. Neither estradiol nor testosterone affected atrial compliance.
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The influence of duration of photoperiod and hemicastration on growth and testicular and endocrine functions of boars.
Yorkshire boars were used to evaluate the influence of duration of photoperiod and hemicastration on growth and testicular and endocrine functions. At 10 wk of age, 5 hemicastrate (HC) and 5 intact (I) boars were assigned to either 8 or 16 hr of light daily until 6 mo of age. Body weights were recorded biweekly throughout the experiment. Venous cannulae were placed in all boars at 6 mo of age, and serum was collected at 30 min intervals from 0800 to 2000 hr. Gonadotropin releasing hormone (GnRH) was infused at 2000 hr (50 micrograms) and at 2030 hr (250 micrograms), and samples of serum were collected until 2400 hr. The following day, all boars were castrated, and the weights and sperm content of the testes and epididymides were determined. At castration, all pigs were given implants containing testosterone. Two weeks later, pigs were again canulated, and serum was obtained at 15 min intervals for 2 hr. Growth of boars was not significantly affected by duration of photoperiod or number of testes. Duration of photoperiod did not affect weight or sperm content of testes or epididymides. Hemi-castrated boars had greater testicular (P less than .01) and capita-corpora (C-C) epididymal weights (P less than .05) and more testicular and C-C sperm (P less than .01) per testis. Neither average concentrations of luteinizing hormone (LH) nor number and amplitude of pulses of LH were affected by photoperiod treatment. However, HC boars had greater average concentrations of LH (P less than .05) than I boars (.71 +/- .05 vs .52 +/- .05 ng/ml). Hemicastrated boars in 16 hr light daily had greater concentrations of FSH in serum (P less than .05) than 8I, 8HC, and 16I boars. Intact and HC boars had similar concentrations of prolactin (PRL) and testosterone. Similarly, concentrations of PRL and testosterone were not affected by duration of photoperiod. Secretion of LH and testosterone after treatment with GnRH was not significantly affected by duration of photoperiod. In general, HC boars released more LH in response to GnRH treatment than I boars. Concentrations of LH were greater (P less than .05) in HC than I boars at .5, 1, 2, and 3 hr after GnRH and tended (P less than .10) to be elevated at 1.5, 2.5, 3.5 and 4 hr after GnRH. The FSH response to GnRH was greater (P less than .05) for 16HC than 8I, 8HC, or 16I boars.(ABSTRACT TRUNCATED AT 400 WORDS)
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Evaluation of relative roles of LH and FSH in regulation of differentiation of Leydig cells using an ethane 1,2-dimethylsulfonate-treated adult rat model.
The relative role of LH and FSH in regulation of differentiation of Leydig cells was assessed using an ethane 1,2-dimethylsulfonate (EDS)-treated rat model in which endogenous LH or FSH was neutralized from day 3 to day 22 following EDS treatment. Serum testosterone and the in vitro response of the purified Leydig cells to human chorionic gonadotropin (hCG) was monitored. In addition RNA was isolated from the Leydig cells to monitor the steady-state mRNA levels by RT-PCR for 17alpha-hydroxylase, side chain cleavage enzyme, steroidogenic acute regulatory protein (StAR), LH receptor, estrogen receptor (ER-alpha) and cyclophilin (internal control). Serum testosterone was undetected and the isolated Leydig cells secreted negligible amount of testosterone on stimulation with hCG in the group of rats that were treated with LH antiserum following EDS treatment. RT-PCR analysis revealed the absence of message for cholesterol side chain cleavage enzyme and 17alpha-hydroxylase although ER-alpha and LH receptor mRNA could be detected, indicating the presence of undifferentiated precursor Leydig cells. In contrast, the effects following deprival of endogenous FSH were not as drastic as seen following LH neutralization. Deprival of endogenous FSH in EDS-treated rats led to a significant decrease in serum testosterone and in vitro response to hCG by the Leydig cells. Also, there was a significant decrease in the steady-state mRNA levels of 17alpha-hydroxylase, cholesterol side chain cleavage enzyme, LH receptor and StAR as assessed by a semiquantitative RT-PCR. These results establish that while LH is obligatory for the functional differentiation of Leydig cells, repopulation of precursor Leydig cells is independent of LH, and also unequivocally establish an important role for FSH in regulation of Leydig cell function.
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[Effects of daidzein on sperm quality, testis gain and testosterone in mice].
OBJECTIVE: To evaluate the effects of daidzein on sperm quality of male mice. METHODS: Three different doses of daidzein were supplemented to pubertal male mice for 21 days(5 mg/kg, 100 mg/kg, 1,000 mg/kg ration). The viability of sperm was determined by eosin-Y, the acrosome was observed by Wright-Giemsa staining, and the testosterone was measured by radioimmunoassay. RESULTS: Daidzein at the dose of 5 mg/kg ration significantly increased serum testosterone levels (P < 0.01), prompted testis gain (P < 0.05), and improved spermatozoa quality. Daidzein at dose of 1,000 mg/kg ration could inhibit the secretion of serum testosterone (P < 0.01), without significant variation in spermatozoa quality. Daidzein at dose of 100 mg/kg ration did not significantly affect sperm quality and other index. CONCLUSIONS: Daidzein can affect sperm quality and in dosage-dependant ways.
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Effects of testosterone, 17beta-estradiol, and downstream estrogens on cytokine secretion from human leukocytes in the presence and absence of cortisol.
Estrogens at physiological concentrations are thought to play an immune-stimulating role, whereas androgens have an anti-inflammatory impact. However, their role on cytokine secretion in the presence or absence of cortisol has not been investigated. Furthermore, the role of hydroxylated estrogens downstream of 17beta-estradiol (E2) on secretion of tumor necrosis factor (TNF) is not known. In this study on peripheral blood leukocytes of healthy male subjects, we scrutinized the influence of prior sex hormones (for 24 h) with and without later addition of cortisol (for another 24 h) on stimulated secretion of TNF, IL-2, IL-4, IL-6, IL-10, and interferon-gamma (IFN-gamma). E2 stabilized or increased immune stimuli-induced secretion of TNF, IL-2, IL-4, IL-6, IL-10, and IFNgamma in relation to testosterone. Testosterone, in contrast, inhibited (IL-2, IL-4, IL-10) or tended to inhibit stimulated secretion of these cytokines (TNF, IFNgamma). This effect of E2 was pronounced at a concentration of 10(-10) M (testosterone: 10(-7) M) in the presence of cortisol. E2 (10(-8) M, 10(-10) M) and testosterone (10(-7) M) did not change glucocorticoid receptor expression. The downstream estrogens 2OH-estradiol(one), 4OH-estradiol(one), and 16OH-estradiol(one) did not stimulate TNF secretion at 10(-10) M, but even inhibited its secretion at 10(-11) M. However, the combination of 16OH-estradiol(one) on one side and 2OH-estradiol(one) or 4OH-estradiol(one) on the other side markedly stimulated TNF secretion that was only observable in the presence of cortisol. In conclusion, at physiological concentrations, E2 and a combination of downstream estrogens stabilized or increased immune stimuli-induced TNF secretion. These effects are dependent on the presence of physiological concentrations of cortisol. This study underlines the proinflammatory role of E2, which is probably dependent on conversion to a proinflammatory cocktail of downstream estrogens and the presence of cortisol.
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