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PubMed1993

Comparison of the effects of pulsatile and constant testosterone on the secretion of gonadotropins in the ram.

The objective of the present study was to compare the effectiveness of a pulsatile vs. a constant pattern of testosterone (T) infusion to suppress LH and FSH secretion in wethers. Two separate experiments were conducted. In Exp 1, animals were subjected to each of four different iv infusion regimens for 3 days: 1) constant diluent, 2) constant T (768 micrograms/kg.24 h), 3) pulsatile (one pulse every 4 h) diluent, and 4) pulsatile T (768 micrograms/kg.24 h). Blood samples were collected at 10-min intervals for 4 h both before infusion and during the last 4 h of the infusion. Compared to diluent, T decreased (P < 0.001) mean LH and increased (P < 0.001) LH interpulse interval. The LH interpulse interval was increased more (P < 0.005) by constant T than by pulsatile T. Mean LH was slightly more suppressed (P = 0.052) by constant T than by pulsatile T. LH pulse amplitude did not differ between constant T and pulsatile T. In Exp 2, animals were subjected to each of three different iv infusion regimens for 4 days: 1) constant diluent, 2) constant T (384 micrograms/kg.24 h), and 3) pulsatile (one pulse every 6 h) T (384 micrograms/kg.24 h). Both LH the interpulse interval (P = 0.001) and LH pulse amplitude (P = 0.04) were increased more by constant T than by pulsatile T. Mean LH was suppressed more (P = 0.002) by constant T than by pulsatile T. In both Exp 1 and 2, none of the treatments significantly affected mean FSH. These results indicate that constant T is more effective than pulsatile T in suppressing LH secretion in the ram.

Animals↗
PubMed1992

Testosterone-LH response and episodic secretion in the male marsupial, Dasyurus viverrinus.

The pattern of testosterone-LH secretion, feedback mechanism, and periodicity of release were investigated in the male marsupial eastern quoll. Testosterone secretion is controlled directly by LH and in the wild, the secretion of both are synchronous and show a major peak at breeding time. An inverse relationship between the secretion of LH and testosterone occurs after castration which supports the hypothesis that a negative feedback mechanism exists between the gonads and the pituitary gland as in other mammals. These hormones fluctuate in a cyclic manner over 24 hr.

Animals↗
PubMed1995

Effects of sex hormones on the steroidogenic activity of dispersed adrenocortical cells of the rat adrenal cortex.

The effect of 17 beta-estradiol and testosterone on glucocorticoid secretion were studied in vitro by using dispersed inner adrenocortical cells obtained from gonadectomized female and male rats. Independently of the sex of animals, estradiol enhanced basal, but not ACTH-stimulated corticosterone (B) secretion; conversely, testosterone inhibited ACTH-stimulated, but not basal B output. HPLC analysis of steroid secreted demonstrated that estradiol induced comparable rises (53-62%) in basal pregnenolone (PREG) and total post-PREG secretion (progesterone, 11-deoxycorticosterone and B). Testosterone inhibited by about 30% ACTH-stimulated PREG production and by about 54% total post-PREG secretion (B was decreased to 56% of the control value, and other steroid hormones were below the limit of sensitivity of our assay system). These findings indicate that sex hormones directly affect rat adrenocortical secretion, mainly by acting on the rate-limiting step of steroidogenesis (i.e. the conversion of cholesterol to PREG); moreover, they suggest that testosterone is also able depress the activity of the enzymes operating distally to cholesterol side-chain cleavage.

Adrenal Cortex↗
PubMed1990

Androgenic deficiency in male rats treated with perfluorodecanoic acid.

Effects of perfluorodecanoic acid (PFDA, 20-80 mg/kg, ip) on the androgenic status of sexually mature male rats were investigated 7 days after treatment. PFDA decreased plasma androgen concentrations in a dose-dependent fashion with an ED50 of approximately 30 mg/kg. The highest dose of PFDA decreased plasma testosterone and 5 alpha-dihydrotestosterone concentrations to 12 and 18%, respectively, of ad libitum-fed control (ALC) values. Secondary to the decreased plasma androgen concentrations were dose-related decreases in the weights and epithelial heights of accessory sex organs. Results from pair-fed control (PFC) rats show that hypophagia in PFDA-treated rats was not a major cause of the low plasma androgen concentrations. When rats were castrated and implanted with testosterone-containing capsules, PFDA-treated and ALC rats had similar plasma testosterone concentrations and secondary sex organ weights. Therefore, the androgenic deficiency in intact PFDA-treated rats does not result from increased plasma clearance of androgens. Rather, PFDA must cause the androgenic deficiency by decreasing the secretion of testosterone from the testis. The decrease in testosterone secretion does not appear to result from a decrease in plasma luteinizing hormone (LH) concentrations, because plasma LH concentrations were not significantly altered by PFDA treatment. This finding suggests that PFDA treatment decreases testicular responsiveness to LH stimulation. The observation that PFDA treatment reduced the secretion of testosterone by testes stimulated in vitro with the LH analog human chorionic gonadotropin demonstrates that this is the case. In addition, since plasma LH concentrations did not increase in response to the low plasma androgen concentrations in PFDA-treated rats, we suggest that PFDA disrupts the normal feedback relationship which exists between plasma androgen and LH concentrations.

Animals↗
PubMed2026

A novel 2D and 3D model for primary adrenocortical carcinoma of advanced and metastasized stage co-secreting cortisol, aldosterone, testosterone, 18-oxocortisol and 18-hydroxycortisol.

Adrenocortical carcinoma (ACC) is a highly aggressive malignancy with poor survival rates and few treatment options. Preclinical models are indispensable to further strengthen our understanding of disease progression and development of novel therapeutic treatments. Here, we report the establishment of a new cell line named ZUC-1 originating from the resection of an advanced primary ACC and its characterization at the genomic, cellular and molecular level. ZUC-1 cells were successfully propagated as monolayer cultures and three-dimensional spheroids. LC-MS/MS analysis revealed for ZUC-1 cells co-secretion of cortisol, aldosterone and testosterone, and the model represented in direct comparison with other current ACC pre-clinical models furthermore significantly elevated expression of SF-1, CYP11B1 and CYP11B2 genes. Whole genome sequencing identified various mutations in genes linked to DNA repair/stress response, stemness, and also steroidogenesis. Interestingly, ZUC-1 represents genotypic and phenotypic variations that might be of interest beyond ACC, including congenital adrenal hyperplasia (CAH) and polycystic ovary syndrome (PCOS). Moreover, 18-oxocortisol and 18-hydroxycortisol release was detected in ZUC-1, conditions which are often linked to hyperaldosteronism, but forskolin, potassium and, at higher concentration, angiotensin II modulability of CYP11B2 for this model is retained. ZUC-1 spheroids exhibited furthermore an intra-spheroidal heterogeneous mix of canonical and non-canonical Wnt pathway activation. We conclude that due to its origin and unique geno- and phenotypes, ZUC-1 represents an intriguing model to further gain a basic understanding of adrenal function, the pathogenesis of ACC, but it might be also of interest in the context of CAH and PCOS.

Humans↗
PubMed1992

A partial characterization of a Sertoli cell-secreted protein stimulating Leydig cell testosterone production.

To examine whether immature rat Sertoli cells in culture secrete a factor(s) which stimulates testosterone production by mature mouse Leydig cells, Sertoli cell-enriched cultures were prepared from 3-week-old male rats with trypsin and collagenase. Sertoli cells were plated at an initial density of 3-5 x 10(6) cells/35 mm well and cultured in 3 ml serum free media supplemented with insulin (10 micrograms/ml). Sertoli cell culture medium (SCCM) collected every 3rd day was added to Leydig cells (10(6) cells in 1 ml of MEM with 2% steroid-free FCS) prepared from 10-week-old mice by mechanical separation and incubated for 3 h at 34 degrees C. Secreted testosterone was determined by RIA. SCCM 15 times concentrated by Amicon YM10 membrane demonstrated a dose-dependent stimulation of testosterone production, whereas there was no effect on testosterone secretion when Leydig cells were maximally stimulated by LH. Leydig cell stimulating activity was retained by both a dialysis membrane with a pore size of 24 A and an ultrafiltration membrane with a molecular weight cut-off of 10 kDa. However, activity was reduced by heating at 60 degrees C for 30 min and almost lost after incubation with 0.1% trypsin for 1 h at 37 degrees C. This activity was not retained by means of a Con A-Agarose column and was demonstrated only in break-through fractions. HPLC gel filtration of a 15 times concentrated SCCM preparation on a TSK gel G3000SW revealed Leydig cell-stimulating activity at approximately 13 kDa.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Ontogeny of gonadotropin, testosterone, and inhibin secretion in normal boys through puberty based on overnight serial sampling.

To investigate hormonal changes occurring in male puberty, we measured LH, FSH, testosterone, and alpha-inhibin immunoactivity in serum samples drawn every 10 min for 8 h (2100-0500 h) from each of 50 normal prepubertal and pubertal boys, aged 8.4-18.8 yr. We measured gonadotropins with ultrasensitive immunofluorometric assays, and testosterone and alpha-inhibin with RIAs. Unlike previous studies, which indexed pubertal development with Tanner stages, we used testicular volume, a more finely graduated indicator of development, to reveal patterns that were obscured when subjects were grouped by Tanner stage. The overnight mean concentration of each hormone increased with testis volume, but the rate of increase on a logarithmic scale slowed as testes grew. Log LH rose precipitously in the late prepubertal and early pubertal periods and plateaued during mid- and late puberty. Based on fitted regression curves, LH increased about 20-fold (from 0.11 IU/L) between testis volumes of 1 and 10 mL, but only an additional 1.5-fold by 30 mL. The developmental trajectory of log testosterone was like that of log LH, but rose less steeply early in puberty. From 0.14 micrograms/L at a testis volume of 1 mL, testosterone increased about 8.5-fold by 10 mL and an additional 3-fold by 30 mL. In contrast, logarithms of overnight mean FSH and alpha-inhibin concentrations rose at a more nearly constant rate throughout puberty. From 0.62 IU/L at a testis volume of 1 mL, the FSH concentration doubled by 10 mL and increased an additional 1.7-fold by 30 mL. From 270 ng/L at a testis volume of 1 mL, inhibin increased 1.5-fold by 10 mL and an additional 1.3-fold by 30 mL. Overnight pulse amplitudes exhibited developmental trajectories similar to those of the corresponding overnight mean concentrations. The number of LH and testosterone pulses during the sampling period averaged 2.2 and 2.1, respectively, at Tanner stage 1 and increased to 4.5 and 3.2, respectively, at Tanner stage 5. The number of FSH and inhibin pulses remained constant throughout puberty, averaging 3.3 and 3.5, respectively. Pairwise correlations among hormone concentrations were strong, reflecting common increasing trends through puberty; however, after accounting for developmental trends, FSH, LH, and testosterone concentrations remained correlated, whereas inhibin was uncorrelated with each of the other three hormones. Measuring gonadotropins with ultrasensitive assays and analyzing the results on a logarithmic scale as a function of testis volume made clear the dramatic hormonal changes that begin before the clinical changes of puberty.

Activity Cycles↗
PubMed1987

Neonatal testosterone modifies LH secretion in the adult female rat by altering the opioid-noradrenergic interaction in the medial preoptic area.

Noradrenergic-opioid interaction in the medial preoptic area (MPOA) was examined in ovariectomised adult rats which were oestrogen-treated and had been injected neonatally with either testosterone propionate (TP) or vehicle (oil). The first experiment involved electrical stimulation of the ventral noradrenergic tract (VNAT) in anaesthetised rats. Blood samples were collected before and after the stimulation to determine plasma levels of luteinising hormone (LH). Approximately half of the animals received naloxone i.v. 15 min before the onset of stimulation. In all groups, stimulation of VNAT elicited a significant increase in plasma LH concentration. However, pretreatment with naloxone in androgenised rats, but not in oil-treated animals, almost doubled the LH increment due to stimulation. Naloxone had no effect on plasma LH concentrations in unstimulated control rats. In the second experiment hypothalamic slices containing the MPOA were preincubated with [3H]noradrenaline [( 3H]NA) and then subjected to electrical field stimulation under the conditions of (a) no drug added and (b, c) morphine superfusion without and with naloxone. The opioid agonist morphine significantly reduced the net release of [3H]NA in normal and TP-treated female rats. Addition of equimolar naloxone reversed this effect in normal females, whereas in the androgenised group it not only reversed this effect but elicited a significant increase in [3H]NA release. From these data we conclude that (1) neonatal testosterone treatment alters noradrenergic-opioid interaction regulating LH secretion in adult females and (2) the site of this change may be the presynaptic opioid input to the noradrenergic terminals in the MPOA.

Animals↗
PubMed1983

Effects of short-term treatment with testosterone on the secretion of FSH and LH in castrated golden hamsters exposed to short days.

Castrated hamsters which were transferred from long (14L:10D) to short (9L:15D) days and received testosterone-filled capsules for 1 week after transfer failed to show a significant suppression in the plasma levels of FSH and LH after capsule removal. In contrast, gonadotrophin concentrations were suppressed in hamsters in which the long-day castration response had been blocked with exogenous testosterone. After castration on long days and exposure to 10 weeks of short days pituitary gland weight and gonadotrophin content, as well as plasma FSH titres, were higher in control animals than in those that had received testosterone implants for 7 weeks of short days. The results suggest that failure of castrated hamsters to respond to the suppressive effects of short days reflects castration-induced changes in hypothalamo-pituitary physiology rather than a neuroendocrine mechanism by which photoperiod modulates gonadotrophin secretion.

Animals↗
PubMed1988

Aromatase inhibition in the dog. I. Effect on serum LH, serum testosterone concentrations, testicular secretions and spermatogenesis.

Chronic treatment of intact male beagles with an orally active nonsteroidal aromatase inhibitor (4-(5,6,7,8-tetrahydroimidazo [1,5a] pyridin-5-yl) benzonitrile hydrochloride; CGS 16949; CIBA-GEIGY) at a dosage of 2.5 mg./kg. per day for six months resulted in increased (p less than 0.01) serum LH and testosterone concentrations compared to placebo-fed controls. The increases in serum LH and testosterone concentrations occurred by one week of treatment and were maintained over the six month period. Testes of CGS 16949A fed dogs obtained at termination of the experiment when perfused in vitro in the presence of a maximally stimulating concentration of LH secreted nondetectable amounts of estradiol and estrone and higher (p less than 0.01) amounts of testosterone, androstenedione and dihydrotestosterone than testes of control dogs. Despite these changes in androgen secretion there was no evidence on any effect of aromatase inhibition upon spermatogenesis. These data support the hypothesis that in the dog, estrogens play a major role in negative feedback of the hypothalamic-pituitary-testicular axis.

Animals↗
PubMed2000

Diurnal rhythms of luteinizing hormone, follicle-stimulating hormone, testosterone, and estradiol secretion before the onset of female puberty in short children.

To investigate hormonal changes before the onset of female puberty, we measured LH and FSH in serum samples drawn every 20 min for 24 h and measured testosterone and estradiol hourly for 24 h. Seventeen girls (13 prepubertal and 4 early pubertal) of short stature, from 5.1-11.4 yr of age, participated in this study. LH and FSH were measured using a time-resolved immunofluorometric assay, and testosterone and estradiol were measured using a sensitivity RIA capable of detecting testosterone and estradiol concentrations of 10 and 2 pg/mL, respectively. Diurnal rhythms of LH, FSH, and testosterone were apparent in all subjects, including those aged 5-6 yr. Serum LH and FSH concentrations showed night-day variation in a pulsatile fashion. The serum testosterone concentration was elevated in the early morning in all subjects. The serum estradiol concentration was elevated in the early morning in 4 of 13 prepubertal subjects and all 4 early pubertal subjects. The diurnal pattern of the serum estradiol concentration was similar to that of the serum testosterone concentration. Mean 24-h LH and testosterone concentrations in prepubertal subjects who did not attain puberty for at least 1 yr were 0.07 U/L and 65 pg/mL, respectively, whereas those in prepubertal subjects who attained puberty within 1 yr (0.14 U/L and 106 pg/mL, respectively) were significantly higher. Furthermore, mean 24-h LH, FSH, testosterone, and estradiol concentrations increased with the onset of puberty. In conclusion, the diurnal rhythms of LH, FSH, and testosterone already exist at 5-6 yr of age, and serum LH and testosterone levels increase before the onset of puberty. These results suggest that preparation for the onset of female puberty may begin in 5- to 6-yr-old girls.

Aging↗
PubMed1985

Radioimmunoassay of 19 nor testosterone. Evidence of its secretion by the testis of the stallion.

Antiserum has been raised in rabbits treated with a 19 nor testosterone-hemisuccinate-bovine-serum-albumin conjugate and used for the development of a specific RIA of plasma 19 nor testosterone. Plasma samples are drawn from testicular and jugular veins of stallions during castration under general anesthesia. Results demonstrate a testicular secretion of 19 nor testosterone and a stress inhibition of this secretion correlatively with stress inhibition of testosterone secretion.

Animals↗