Possible role of prolactin in the inhibitory effect of testosterone on the hypothalamic-pituitary-testicular axis in the rat

1985 ◽  
Vol 105 (3) ◽  
pp. 423-427 ◽  
Author(s):  
J. A. F. Tresguerres ◽  
L. F. Perez Mendez ◽  
A. Lopez-Calderon ◽  
A. I. Esquifino

ABSTRACT To study the role of testosterone on the regulation of the hypothalamic-pituitary-testicular axis, young intact male Wistar rats were given acute (24 h) or chronic (5 days) subcutaneous treatments of 500 μg testosterone propionate (TP) or vehicle alone. Plasma LH, prolactin and testosterone levels were measured both basally and after administration of LH-releasing hormone (LHRH) or human chorionic gonadotrophin (hCG) by means of specific radioimmunoassay systems using materials supplied by the NIADDK. After acute treatment with TP there was an increase in basal plasma testosterone concentrations and no modification in the hCG response when compared with vehicle-treated animals. No difference could be detected in basal plasma testosterone levels after the chronic treatment, but a significant reduction in the hCG response was observed. Both acute and chronic treatments with TP resulted in a significant decrease of basal plasma LH levels. A reduced LH response to LHRH in acutely treated rats and no response in the chronically treated rats was detected. Plasma prolactin levels showed an increase after both acute and chronic treatments. To evaluate the possible role of the increased plasma prolactin levels on the above modifications during TP treatment, another group of animals was treated with TP and bromocriptine (dopamine agonist) simultaneously to avoid the increase in plasma prolactin levels. In this situation, neither basal plasma LH levels nor the response to LHRH were altered when compared to vehicle-treated rats; a normal testosterone response to hCG stimulation was observed in spite of the high basal plasma testosterone levels. All these observations suggest that increased prolactin levels may exert a modulatory role on the negative feedback effect of testosterone both at the testicular and central levels. J. Endocr. (1985) 105, 423–427

1981 ◽  
Vol 96 (2) ◽  
pp. 273-280 ◽  
Author(s):  
Mridula Chowdhury ◽  
Robert Tcholakian ◽  
Emil Steinberger

Abstract. It has been suggested that treatment of intact male rats with oestradiol benzoate (OeB) causes an interference with testosterone (T) production by the testes by a direct inhibitory effect on steroidogenesis. To test this hypothesis, different doses (5, 10 or 25 IU) of hCG were administered concomitantly with 50 μg of OeB to adult intact or hypophysectomized male rats. The testicular and plasma testosterone, and serum hCG levels were determined. The sex accessory weights were recorded. In the intact OeB-treated group of animals, hCG stimulated both the secondary sex organs and plasma testosterone levels above the intact control group. However, in hypophysectomized animals, although plasma testosterone levels increased above that of intact controls, their secondary sex organ weights did not. Moreover, inspite of high circulating hCG levels, the testicular testosterone content and concentration remained suppressed in OeB-treated animals. The reason for such dichotomy of hCG action on OeB-treated animals is not clear at present.


1974 ◽  
Vol 63 (2) ◽  
pp. 325-335 ◽  
Author(s):  
R. P. MICHAEL ◽  
K. D. R. SETCHELL ◽  
T. M. PLANT

SUMMARY The assays of testosterone and corticosteroids in plasma from adult male rhesus monkeys using competitive protein-binding and radioimmunoassay techniques are described. The radioimmunoassay for testosterone was conducted without chromatography and, therefore, additionally estimated 17β-hydroxy-5α-androstan-3-one (dihydrotestosterone). Levels of testosterone in the peripheral plasma of 14 intact male rhesus monkeys showed marked fluctuations over a period of 24 h. Concentrations of testosterone at 22.00 h (1776 ± 814 ( ± s.d.) ng/100 ml) were approximately double those at 08.00 h (858 ± 407 ng/100 ml), 12.00 h (898 ± 316 ng/100 ml) and 16.00 h (784 ± 530 ng/100 ml). Castration resulted in low plasma testosterone levels (85 ± 29 ng/100 ml), and the increases at 22.00 h were no longer observed. In intact males, the 'basal' plasma corticosteroidlevel(08.00 h) was 22·4 ± 6·0 μg/100 ml. Administration of synthetic corticotrophin raised plasma corticosteroid levels without changing plasma testosterone concentration. Because plasma testosterone levels were not related to changes in adrenocortical activity, the noctural rises appear to be due to changes in testicular secretion.


1971 ◽  
Vol 68 (3) ◽  
pp. 576-584 ◽  
Author(s):  
K. O. Nilsson ◽  
B. Hökfelt

ABSTRACT Metyrapone was administered either orally, 750 mg every four h, in a total of six doses, or intravenously 30 mg per kg body weight as a four h infusion. In three males with normal endocrine functions, metyrapone given orally or intravenously induced a fall in plasma testosterone and an elevation of androstenedione within 2–8 h. When metyrapone was administered to a patient given dexamethasone to suppress endogenous ACTH production, the androstenedione levels did not alter whereas the testosterone levels showed a slight, transient decrease. In two normal females metyrapone administration was followed by a marked increase in plasma androstenedione whereas testosterone showed only a minor, gradual increase. In one male patient with Addison's disease the basal plasma testosterone was normal whereas the level of androstenedione was low. Following metyrapone intravenously, there was a slight suppression of plasma testosterone but no change in the androstenedione concentration. In one patient with primary hypogonadism, two with secondary hypogonadism and two with Klinefelter's syndrome the plasma testosterone was low under basal conditions and did not change following metyrapone. Basal plasma androstenedione was within the range for normal males and increased markedly following metyrapone in all the cases.


1992 ◽  
Vol 132 (3) ◽  
pp. 449-459 ◽  
Author(s):  
B. Pérez-Villamil ◽  
E. Bordiú ◽  
M. Puente-Cueva

ABSTRACT We have investigated the role of physiological prolactin levels in the development of prepubertal male rats. Prolactin GH and testosterone levels, as well as body, ventral prostate and testicular weight, have been analysed in both control and bromocriptine-treated rats between 21 and 60 days of life. Furthermore the role of prolactin in the regulation of its own receptors has also been studied during the same period. In control rats, prolactin levels showed a prepubertal peak of secretion at 25 days of age. At this time GH and testosterone levels were low and did not show any significant variation. After this age, prolactin levels increased more gradually; determinations of GH showed great variation with low levels in most of the rats and very high values in the other animals; testosterone levels remained low until day 35 after which they increased. Simultaneously with the serum prolactin peak on day 25, a decrease in prolactin-binding capacity of ventral prostate glands, was observed and a maximum rate of body, prostate and testicular weight gain was obtained. Furthermore, in rats with pharmacologically suppressed serum prolactin levels (lower than 1 μg/l), prolactin binding to prostate glands as well as the weight of body, ventral prostate and testes were lower than in control animals. When results were expressed in mg prostate or testes/g body weight, testes from 25-day-old treated rats weighed significantly less than controls. The later stages of development, from days 25 to 60, were characterized by an initial decline in serum prolactin levels at 29 days of age which was followed by a continuous increase until adult values were reached. During this period, prostatic prolactin receptors which were at their lowest value at 33 days of age showed a gradual rise parallel with the observed increase in plasma prolactin levels. When testicular tissue was analysed, no changes in prolactin-binding sites caused by sexual maturation were observed. The present results indicate that physiological prolactin secretion has a specific effect on the normal increase in the prostate, testes and body weight and clearly is also implicated in the regulation of its prostatic receptors at the earlier stages of development. Journal of Endocrinology (1992) 132, 449–459


1974 ◽  
Vol 77 (4) ◽  
pp. 753-764 ◽  
Author(s):  
A. G. H. Smals ◽  
P. W. C. Kloppenborg ◽  
Th. J. Benraad

ABSTRACT The effect of acute (1500 IU/day for 3 days) and chronic HCG administration (1500 IU, 3 times weekly) on plasma testosterone levels in patients with Klinefelter's syndrome was compared with the response observed in patients with hypogonadotrophic eunuchoidism and in eugonadal male controls. Basal plasma testosterone levels in the Klinefelter patients were significantly lower than in the control subjects and significantly higher than in the patients with secondary hypogonadism. In all but one Klinefelter patient the plasma LH levels were markedly elevated even in the presence of normal testosterone levels. No significant correlation could be demonstrated between the plasma testosterone concentrations and the LH levels in the Klinefelter patients. Short term HCG administration resulted in a significant increase in the plasma testosterone levels in each of the 3 groups studied, independent of the basal value. The absolute increase in the Klinefelter patients was quantitatively comparable to that in the patients with secondary hypogonadism, but significantly lower than in the eugonadal controls. During long term HCG treatment the plasma testosterone levels definitely increased in both patient groups, but remarkably in the Klinefelter patients testosterone levels tended to decrease on continuing treatment, though in most patients testosterone levels remained higher than the pre-treatment values. The data on the effect of acute and chronic HCG administration on plasma testosterone levels in this study illustrate again that Leydig cells in Klinefelter's syndrome still retain a functional reserve, though less than in eugonadal males.


2020 ◽  
Author(s):  
Erin Sundermann ◽  
Matthew S. Panizzon ◽  
Xu Chen ◽  
Murray Andrews ◽  
Douglas Galasko ◽  
...  

Abstract Women show greater pathological Tau biomarkers than men along the Alzheimer’s disease (AD) continuum, particularly among apolipoprotein ε-E4 (APOE4) carriers; however, the reason for this sex difference in unknown. Sex differences often indicate an underlying role of sex hormones. We examined whether testosterone levels might influence this sex difference and the modifying role of APOE4 status. Analyses included 172 participants (25 cognitively normal, 97 mild cognitive impairment, 50 AD participants) from the Alzheimer’s Disease Neuroimaging Initiative (34% female, 54% APOE4+, aged 55–90). We examined the separate and interactive effects of plasma testosterone levels and APOE4 on cerebrospinal fluid phosphorylated-tau181 (p-Tau) levels in the overall sample, and the sex difference in p-Tau levels before and after adjusting for testosterone. A significant APOE4-by-testosterone interaction revealed that lower testosterone levels related to higher p-Tau levels among APOE4 carriers regardless of sex. As expected, women had higher p-Tau levels than men among APOE4 carriers only, yet this difference was eliminated upon adjustment for testosterone. Results suggest that testosterone is protective against p-Tau particularly among APOE4 carriers. The lower testosterone levels that typically characterize women may predispose them to pathological Tau, particularly among female APOE4 carriers.


1989 ◽  
Vol 120 (2) ◽  
pp. 269-273 ◽  
Author(s):  
A. López-Calderón ◽  
C. Ariznavarreta ◽  
M. D. Calderón ◽  
J. A. F. Tresguerres ◽  
M. I. Gonzalez-Quijano

ABSTRACT The response of prolactin to chronic stress in intact, adrenalectomized and adrenomedullectomized male rats was studied. Immobilization stress in intact animals induced a significant increase in plasma concentrations of prolactin after 20 and 45 min and a significant decrease when the rats were submitted to chronic restraint (6 h daily for 4 days). Five weeks after adrenomedullectomy, plasma prolactin and corticosterone responses to chronic stress were not modified. In contrast, the inhibitory effect of chronic stress on prolactin secretion was totally suppressed by adrenalectomy. When treated with dexamethasone during the 4 days of restraint, adrenalectomized stressed rats showed similar plasma concentrations of prolactin to the intact stressed rats. These data indicate that the adrenal cortex is able to play an inhibitory role on prolactin secretion during stress only through a prolonged release of glucocorticoids. Journal of Endocrinology (1989) 120, 269–273


2010 ◽  
Vol 2010 ◽  
pp. 1-11 ◽  
Author(s):  
José Sereno ◽  
Belmiro Parada ◽  
Flávio Reis ◽  
Fernanda X. Cunha ◽  
Edite Teixeira-Lemos ◽  
...  

To evaluate the effect of a cyclooxygenase 2 inhibitor, celecoxib (CEL), on bladder cancer inhibition in a rat model, when used as preventive versus as curative treatment. The study comprised 52 male Wistar rats, divided in 5 groups, during a 20-week protocol: control: vehicle, carcinogen: 0.05% ofN-butyl-N-(4-hydroxybutyl) nitrosamine (BBN), CEL: 10 mg/kg/day of the selective COX-2 inhibitor Celebrex, preventive CEL (CEL+BBN-P), and curative CEL (BBN+CEL-C) groups. Although tumor growth was markedly inhibited by the preventive application of CEL, it was even aggravated by the curative treatment. The incidence of gross bladder carcinoma was: control 0/8(0%), BBN 13/20(65%), CEL 0/8(0%), CEL+BBN-P 1/8(12.5%), and BBN+CEL-C 6/8(75%). The number and volume of carcinomas were significantly lower in the CEL+BBN-P versus BBN, accompanied by an ample reduction in hyperplasia, dysplasia, and papillary tumors as well as COX-2 immunostaining. In spite of the reduction of tumor volumes in the curative BBN+CEL-C group, tumor malignancy was augmented. An anti-inflammatory and antioxidant profile was encountered only in the group under preventive treatment. In conclusion, preventive, but not curative, celecoxib treatment promoted a striking inhibitory effect on bladder cancer development, reinforcing the potential role of chemopreventive strategies based on cyclooxygenase 2 inhibition.


1974 ◽  
Vol 77 (2) ◽  
pp. 387-400 ◽  
Author(s):  
A. G. H. Smals ◽  
P. W. C. Kloppenborg ◽  
T. J. Benraad

ABSTRACT Basal plasma testosterone levels (mean ± sd 290 ± 141 ng/100 ml) (range 72–684 ng/100 ml) in 25 chromatin positive patients with Klinefelter's syndrome (23 XXY, 1 XXYY, 1 XY/XXY) were significantly lower than in 25 age matched controls (mean ± sd 603 ± 169 ng/100 ml). In 11 out of the 25 Klinefelter patients however, plasma testosterone levels were in the normal range and these patients differed significantly from the patients with low testosterone levels with respect to the clinical state of androgenicity. In the group of Klinefelter patients, but not in the controls, a significant negative correlationship was found between plasma testosterone levels and each of the variables: body weight, arm span, length of the lower body segment and the ratio's lower/upper and span/upper body segment.


1977 ◽  
Vol 86 (3) ◽  
pp. 641-650 ◽  
Author(s):  
Dominique Gendrel ◽  
Marc Roger ◽  
Jean-Louis Chaussain ◽  
Pierre Canlorbe ◽  
Jean-Claude Job

ABSTRACT LH-RH test and HCG stimulation test were performed in 154 cryptorchid boys aged 1 month to 15 years (64 unilateral and 90 bilateral). Basal plasma LH levels and LH response to LH-RH were significantly lower from infancy to early puberty in cryptorchids compared with controls. Basal FSH levels and FSH response to LH-RH were normal. The post-HCG rise of plasma testosterone was reduced until mid-puberty. A significant positive correlation was found between post-HCG testosterone levels and pre- and post-LH-RH levels of LH. This correlation suggests that testicular maldescent and the decreased ability of Leydig cells to respond to a short course of HCG may result from an early defect or a delay of pituitary LH secretion.


Sign in / Sign up

Export Citation Format

Share Document