Oestrogenic regulation of testicular androgen production during development in the rat

1985 ◽  
Vol 105 (2) ◽  
pp. 211-218 ◽  
Author(s):  
B. A. Keel ◽  
T. O. Abney
Keyword(s):  
Serum Testosterone ◽  
Male Rats ◽  
Serum Prolactin ◽  
Testicular Function ◽  
Intact Male ◽  
Oestrogen Treatment ◽  
Testosterone Production ◽  
Age Related ◽  
Serum Lh

ABSTRACT The influence of age on the sensitivity of the testis to oestrogens was investigated. Intact male rats at 10, 25, 40 and 53 days of age were injected s.c. with vehicle, 5 or 50 μg oestradiol or diethylstilboestrol (DES)/100 g body wt twice daily for 2 days; the animals were killed 12 h after the last injection. Subsequently, the concentrations of testicular androgens and serum LH, prolactin, testosterone and androstanediol (5α-androstane-3α, 17β-diol) were measured. Testicular androgen production was determined in vitro in the presence or absence of human chorionic gonadotrophin (hCG) or dibutyryl cyclic AMP (dbcAMP). Androgens in the serum and testes displayed an age-related alternating pattern with androstanediol being the major androgen produced at 27 days of age. As a result of oestrogen treatment, serum LH concentrations were decreased while serum prolactin was increased. Serum testosterone was decreased by 36–55% in the 12-day-old group and further reduced by 95% of control values by day 55; serum androstanediol was less sensitive to oestrogen suppression. Testicular concentrations of both testosterone and androstanediol exhibited a marked reduction in 12-day-old animals as a result of oestrogen administration. These values were reduced by 85–95% at day 27 and remained suppressed even at 55 days. Basal production of testosterone was unaffected by oestrogen treatment in 12- and 27-day-old animals but was markedly decreased by day 42. Significant suppression of basal production of androstanediol was observed as early as day 12. Oestradiol treatment caused a significant reduction in hCG responsiveness of both androgens at days 12, 42 and 55. Oestrogen administration resulted in a significant (32–59%) decline in dbcAMP-responsive testosterone production in the 42-day group and a further suppression in the 55-day group. A marked inhibition of dbcAMP-stimulated androstanediol production was also observed in the 42- and 55-day groups. Testosterone production in response to dbcAMP was not significantly altered in the 12- and 27-day groups. With few exceptions the effects of oestradiol and DES on testicular function were similar. The data presented here suggest that the inhibitory effects of oestrogens become more pronounced as the animal approaches adulthood, that oestradiol and DES are similarly effective in regulating testicular function at all ages studied and that the production of both testosterone and androstanediol are suppressed by oestrogen administration. J. Endocr. (1985) 105, 211–218

Hyperprolactinaemia attenuates the gonadotrophin releasing hormone receptor response to gonadectomy in rats

1982 ◽  
Vol 95 (2) ◽  
pp. 267-274 ◽  
Author(s):  
R. N. Clayton ◽  
L. C. Bailey
Keyword(s):  
Female Rats ◽  
Male Rats ◽  
Serum Prolactin ◽  
Intact Male ◽  
Adult Rats ◽  
Releasing Hormone ◽  
Receptor Response ◽  
Serum Lh ◽  
Gonadotrophin Releasing Hormone ◽  
Qualitative Index

Measurement of pituitary gonadotrophin releasing hormone (Gn-RH) receptor content provides a qualitative index of prior exposure of the pituitary gland to endogenous Gn-RH. The effect of moderate hyperprolactinaemia (serum prolactin = 95–250 μg/l), achieved with three pituitary grafts beneath the renal capsule, on the pituitary Gn-RH receptor content and serum LH responses to gonadectomy of adult rats has been studied. In males the presence of hyperprolactinaemia for 7 days completely prevented the increase in Gn-RH receptor content 3 days after castration and inhibited the serum LH rise by 45%. By 6 days after castration, Gn-RH receptors had increased in the hyperprolactinaemic castrated animals but values were 33% lower than in sham-grafted controls, while the serum LH increase was attenuated by 30%. Pituitary LH content was also lower in grafted castrated animals 6 days after castration. Hyperprolactinaemia for 3 weeks had no effect on Gn-RH receptors or pituitary LH content of intact male rats, although basal serum LH was decreased by 50%. Hyperprolactinaemia also attenuated the increases in Gn-RH receptors, serum LH and pituitary LH which occurred 6 days after ovariectomy in female rats. In all experiments the pituitary content of prolactin was reduced by 80–90% in animals bearing pituitary grafts. These results suggest that hyperprolactinaemia restricts the Gn-RH receptor response to gonadectomy by decreasing endogenous hypothalamic Gn-RH secretion.

Age-related differences in the growth hormone secretory response to hGHRH 1-44 in male rats from infancy through puberty

1987 ◽  
Vol 116 (1) ◽  
pp. 138-144 ◽  
Author(s):  
Dorothy I. Shulman ◽  
Margaret Sweetland ◽  
Gregory Duckett ◽  
Allen W. Root
Keyword(s):  
Serum Testosterone ◽  
Pituitary Cell ◽  
Secretory Response ◽  
Male Rats ◽  
Percentage Increase ◽  
Gh Secretion ◽  
Age Related ◽  
Pentobarbital Anaesthesia

Abstract. The GH secretory response to varying doses (15, 30, 60 μg/kg) of sc administered hGHRH 1–44 (or normal saline) was measured in vivo in 10, 20, 30, 40, 50, 60 and 130 days old pentobarbital-anaesthetized, male rats. The 10-min GH level and ΔGH were in general significantly greater in older rats (50, 60, 130 days old) than in younger rats (10, 20 days old) following all doses hGHRH. Ten-day-old animals had no significant GH response to any dose of hGHRH tested. ΔGH correlated significantly with age (r = 0.36; P < 0.0001) and Sm-C level (r = 0.29; P < 0.01) but not with serum testosterone concentrations. Monolayer pituitary cell cultures were established in rats aged 10 to 130 days and were incubated with varying concentrations of hGHRH 1–44 (0.05, 0.5, 5.0, 50 nmol/l or incubation medium). Cultures from 10- and 20-day-old animals had a greater percentage increase over basal GH secretion than other groups at all concentrations of hGHRH tested (P < 0.05). Age-related differences in the GH secretory response to hGHRH are present in male rats from 10 to 130 days. The in vitro results reported here suggest that the increase in magnitude and sensitivity of the GH response to hGHRH observed in pubertal animals in vivo under pentobarbital anaesthesia is likely due to influences above the level of the somatotrope receptor.

Investigations upon the mechanism of inhibition of spermatogenesis in the rat by a dimeric ethynodiol-testosterone ester

1988 ◽  
Vol 117 (4) ◽  
pp. 536-544 ◽  
Author(s):  
Hans-Joachim Born ◽  
Petra Hörster-Poschmann ◽  
Wilfried Stoll ◽  
Jürgen Sandow ◽  
Hans-Dieter Taubert ◽  
...  
Keyword(s):  
Serum Testosterone ◽  
Normal Serum ◽  
Male Rats ◽  
Serum Testosterone Level ◽  
Intact Male ◽  
Strong Suppression ◽  
Mechanism Of Inhibition ◽  
Serum Lh ◽  
Minor Significance ◽  
Androgen Binding

Abstract. The combination of androgens and progestogens has been shown to be a suitable male contraceptive. Previous experiments revealed that injection of a dimeric testosterone-ethynodiol ester into rats and monkeys induces azoospermia for several weeks. In order to investigate the mechanism of action, we compared the endocrine effects of a single injection of 10 mg of the dimeric ester into intact male rats with that of 6 mg of norethisterone enanthate + 6 mg of testosterone enanthate. After the injection of the dimer there was a transitory reduction of serum FSH and a strong suppression of serum LH and testosterone, of testicular testosterone and of androgen-binding protein (ABP) in the testis and epididymis for at least 8 weeks, whereas spermatogenesis was totally depressed between the 4th and 8th week. Contrary to this, the enanthates caused only a slight suppression of spermatogenesis, although serum LH, testicular testosterone and ABP were profoundly reduced. The only conspicuous difference in the endocrine pattern of both groups during the first 4 weeks was in the serum testosterone level which remained normal in the rats treated with the enanthates. The results suggest that testicular testosterone and ABP concentrations are of minor significance for an intact spermatogenesis, and that some other factors produced by Sertoli cells might be involved and possibly maintained by normal serum testosterone levels.

OESTROGEN INDUCED LEYDIG CELL REFRACTORINESS TO GONADOTROPHIN STIMULATION

1978 ◽  
Vol 89 (2) ◽  
pp. 379-392 ◽  
Author(s):  
J. M. Saez ◽  
F. Haour ◽  
B. Loras ◽  
P. Sanchez ◽  
A. M. Cathiard
Keyword(s):  
Dna Synthesis ◽  
Binding Sites ◽  
Interstitial Cells ◽  
Male Rats ◽  
Plasma Testosterone ◽  
Camp Content ◽  
Oestrogen Treatment ◽  
Testosterone Production

ABSTRACT In vivo administration of oestradiol to male rats modifies plasma LH, FSH and testosterone levels, cAMP and testosterone production and DNA synthesis in isolated interstitial cells. Intramuscular injection of oestradiol benzoate (Oe2B) at the dose of 1 or 100 μg/day for 6 days induced a 5- and 10-fold decrease in plasma testosterone, respectively, and a 2-fold decrease in plasma LH and FSH. Plasma testosterone was already significantly decreased 2 h after the Oe2B injection at which point the plasma LH and FSH levels were not yet significantly decreased. In vivo steroidogenic responsiveness to hCG evaluated by plasma and testicular contents was already significantly lower than that of controls 2 h following oestradiol administration. Thereafter response to hCG progressively decreased during the 6 days of 1 or 100 μg oestradiol treatment, reaching 30 and 10 %, respectively, of that of controls on the last day. On the contrary the testicular cAMP content 2 h after hCG injection was significantly higher in oestradiol treated animals than in controls after 24 h. The number of hCG binding sites in isolated Leydig cells decreased to approximately 50 % of that of controls on days 3 to 6 following Oe2B treatment. In vitro testosterone production by isolated interstitial cells, either under basal conditions or under stimulation by hCG or N6O2 dibutyryl adenosine 3′,5′-monophosphate (DbcAMP), was lowered as early as 2 h following the injection of Oe2B to the animals. From 1 to 6 days following Oe2B administration, testosterone secretion, in response to both stimuli, was approximately 4 times lower than that of the control animals. Paradoxically, by the second day of oestrogen treatment, basal and hCG induced in vitro cAMP production by interstitial cells was significantly higher than controls despite a significant decrease in the number of binding sites. The incorporation of thymidine into interstitial cells DNA were decreased following 2 days of oestrogen administration. However, the conversion of pregnenolone to testosterone was unchanged. These inhibitory effects of oestradiol were not overcome by simultaneous administration of hCG. These results strongly suggest that the rapid inhibitory action of oestradiol on interstitial cell function, steroidogenesis, and DNA synthesis, occurs at the testicular level. Changes observed in gonadotrophin receptor sites or in plasma LH levels may have a long term effect on the steroidogenic refractoriness to hCG. However this refractoriness is primarily related to an abnormality of some step of steroidogenesis beyond cAMP formation.

Effect of oestrogen treatment on gonadotroph function in adult male rats

1987 ◽  
Vol 114 (1) ◽  
pp. 95-101 ◽  
Author(s):  
G. Saade ◽  
D. R. London ◽  
R. N. Clayton
Keyword(s):  
Adult Male ◽  
Term Treatment ◽  
Male Rats ◽  
Ovariectomized Rats ◽  
Serum Prolactin ◽  
Control Group ◽  
Oestrogen Treatment ◽  
Serum Lh ◽  
Long Term Treatment

ABSTRACT The effect of oestradiol-17β on the hypothalamo-pituitary axis of intact adult male rats was studied. A single injection of oestradiol did not change the serum LH response to gonadotrophin-releasing hormone (GnRH) 48 h or 7 days after the injection, while administration of oestrogen over 66 days suppressed basal serum LH to <3·1 μg/l and did not enhance the LH response to GnRH at any time. Treatment of ovariectomized rats with oestradiol capsules, however, enhanced the LH response to GnRH on days 3 and 14 of the treatment as compared with the control group (P<0·02 and P<0·05 respectively). Long-term treatment with oestradiol suppressed intrapituitary LH and FSH contents as well as pituitary GnRH receptors (P<0·0004, P<0·005 and P<0·001 respectively), whereas serum and intrapituitary prolactin levels were increased. To exclude the possible inhibitory effect of hyperprolactinaemia on LH responsiveness to GnRH, oestradiol-implanted rats were treated with bromocriptine. This prevented the rise in serum prolactin, but failed to enhance the LH response to GnRH. Neither short- nor long-term treatment with oestradiol given under conditions shown to be effective in female animals stimulated the hypothalamo-pituitary-gonadotrophin axis in adult male rats. J. Endocr. (1987) 114,95–101

Effects of in vivo gonadal hormone environment on in vitro hGRF-40-stimulated GH release

1985 ◽  
Vol 249 (3) ◽  
pp. E276-E280 ◽  
Author(s):  
W. S. Evans ◽  
R. J. Krieg ◽  
E. R. Limber ◽  
D. L. Kaiser ◽  
M. O. Thorner
Keyword(s):  
Female Rats ◽  
Male Rats ◽  
Gonadal Hormone ◽  
Base Line ◽  
Pituitary Cells ◽  
Intact Male ◽  
Castrate Male ◽  
Basal Release

The effects of gender and the gonadal hormone environment on basal and stimulated growth hormone (GH) release by dispersed and continuously perifused rat anterior pituitary cells were examined. Cells from intact male and diestrus day 2 female rats and from castrate male rats either untreated or treated with testosterone (T) or 17 beta-estradiol (E2) were used. Basal GH release (ng/min per 10(7) cells; mean +/- SE) by cells from diestrus day 2 female rats was less than by cells from castrate rats treated with T (4.3 +/- 0.6 vs. 11.4 +/- 2.7, respectively; P less than 0.025). No other differences in basal release were detected. Concentration-response relationships were documented between human GH-releasing factor 40 (hGRF-40; 0.03-100 nM given as 2.5-min pulses every 27.5 min) and GH release. Mean (+/- SE) overall GH release (ng/min per 10(7) cells) above base line was greater by cells from intact male rats (496 +/- 92) than by cells from castrate (203 +/- 37.3; P less than 0.0001), castrate and T-treated (348 +/- 52.8; P = 0.008), or castrate and E2-treated (58.1 +/- 6.8; P less than 0.001) male rats or by diestrus day 2 rats (68.6 +/- 9.5; P = 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)

In vivo effects of flavonoid EMD 21388 on thyroid hormone secretion and metabolism in rats

1991 ◽  
Vol 261 (2) ◽  
pp. E227-E232 ◽  
Author(s):  
J. P. Schroder-van der Elst ◽  
D. van der Heide ◽  
J. Kohrle
Keyword(s):  
Thyroid Hormone ◽  
Hormone Secretion ◽  
Male Rats ◽  
Intact Male ◽  
Hormone Production ◽  
Iodide Uptake ◽  
Brown Adipose ◽  
In Vivo Effects

In vitro, the synthetic flavonoid EMD 21388 appears to be a potent inhibitor of thyroxine (T4) 5'-deiodinase and diminishes binding of T4 to transthyretin. In this study, in vivo effects of long-term administration of EMD 21388 on thyroid hormone production and metabolism were investigated. Intact male rats received EMD 21388 (20 mumol.kg body wt-1.rat-1.day-1) for 14 days. [125I]T4 and 3,5,3'-[131I]triiodotyronine (T3) were infused continuously and intravenously in a double-isotope protocol for the last 10 and 7 days, respectively. EMD 21388 decreased plasma thyroid hormone concentrations, but thyrotropin levels in plasma and pituitary did not change. Plasma clearance rates for T4 and T3 increased. Thyroidal T4 secretion was diminished, but T3 secretion was elevated. Extrathyroidal T3 production by 5'-deiodination was lower. T4 concentrations were markedly lower in all tissues investigated. Total tissue T3 was lower in brown adipose tissue, brain, cerebellum, and pituitary, tissues that express the type II 5'-deiodinase isozyme due to decreased local T3 production. Most tissues showed increased tissue/plasma ratios for T4 and T3. These results indicate that this flavonoid diminished T4 and increased T3 secretion by the thyroid, probably in analogy with other natural flavonoids, by interference with one or several steps between iodide uptake, organification, and hormone synthesis.

Androgen regulation and site specificity of angiotensinogen gene expression and secretion in rat adipocytes

2000 ◽  
Vol 279 (6) ◽  
pp. E1398-E1405 ◽  
Author(s):  
Valérie Serazin-Leroy ◽  
Mireille Morot ◽  
Philippe de Mazancourt ◽  
Yves Giudicelli
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Mrna Expression ◽  
Protein Secretion ◽  
Male Rats ◽  
Fat Cells ◽  
Intact Male ◽  
Rat Adipocytes ◽  
Fat Deposits

Adipose tissue is an important source of angiotensinogen (ATG), and hypertension is commonly associated with android obesity. Therefore, we tested the hypothesis that androgens may control ATG gene expression and secretion in rat fat cells. In intact male rats, ATG mRNA expression (Northern blot and co-reverse transcription-polymerase chain reaction analysis) and protein secretion were significantly higher in deep intra-abdominal (perirenal and epididymal) than in subcutaneous adipocytes. After castration, ATG mRNA was reduced almost 50% in the three fat deposits, with parallel changes in ATG protein secretion. Conversely, testosterone treatment fully restored the ATG mRNA decrease after castration, whatever the anatomical origin of the adipocytes. Finally, a 24-h in vitro exposure of perirenal fat cells or differentiated preadipocytes from castrated rats to testosterone or dihydrotestosterone (10 nM free hormone concentration) increased ATG mRNA expression by 50–100%, an effect that was prevented by the anti-androgen cyproterone acetate. These data, demonstrating both in vivo and in vitro androgen induction of ATG mRNA expression in rat adipocytes, add further weight to the hypothesis of a link between adipose tissue ATG production, androgens, and android obesity-related hypertension.

Hypothalamic-pituitary-testicular function in rats after supraphysiological doses of a highly active LRH analogue (buserelin)

1980 ◽  
Vol 94 (4) ◽  
pp. 489-497 ◽  
Author(s):  
J. Sandow ◽  
W. v. Rechenberg ◽  
G. Jerzabek ◽  
K. Engelbart ◽  
H. Kuhl ◽  
...  
Keyword(s):  
Organ Distribution ◽  
Testicular Function ◽  
Testosterone Production ◽  
Highly Active ◽  
Group I ◽  
End Of Treatment ◽  
Liver And Kidney ◽  
Lh Release ◽  
Dose Levels

Abstract. Male pre-pubertal rats (60 g) were treated with the LRH analogue, [D-Ser(But)6]LRH(1—9)-nonapeptide-ethylamide (buserelin, Hoe 766), during 4 weeks by daily sc injections of 5, 50 or 500 ng peptide (group I, II and III). At the end of treatment, hypothalamic LRH content and arylamidase activity (LRH degrading enzyme) were not changed. Pituitary arylamidase activity was reduced, but the pituitary LRH receptors (tested by analogue binding in vitro) were not diminished. Pituitary accumulation of [125I]buserelin 60 min after iv injection was not modified and organ distribution in liver and kidney was unchanged. Pituitary responsiveness to the analogue was reduced at the highest dose, but there was significant LH-release at all three dose levels. Testosterone production in vitro (stimulated by hCG) was unaltered in group I and dramatically reduced in group II and III. Testicular testosterone content and hCG binding by testes homogenates were dose-dependently reduced. Histology of the testes after 4 weeks treatment showed minimal impairment of spermatogenesis at the highest dose, whereas the epididymis was almost devoid of sperm. The results indicate, that low dose treatment with a highly active LRH analogue, buserelin, does not interfere with pituitary responsiveness (LRH receptors and LH-release) and testicular function (testosterone production, testosterone content, LH-receptor level). At higher doses, pituitary and testicular responsiveness are dose-dependently inhibited. At the pituitary level, LRH receptors were not reduced. The antifertility effect of supraphysiological doses at the testicular level is explained by an LH-dependent loss of LH-receptors.

ANNUAL RHYTHMS OF LUTEINIZING HORMONE, FOLLICLE-STIMULATING HORMONE, PROLACTIN AND TESTOSTERONE IN THE SERUM OF MALE RHESUS MONKEYS

1979 ◽  
Vol 83 (2) ◽  
pp. 131-139 ◽  
Author(s):  
W. BECK ◽  
W. WUTTKE
Keyword(s):  
Rhesus Monkeys ◽  
Serum Testosterone ◽  
Serum Levels ◽  
Serum Prolactin ◽  
First Year ◽  
Thyrotrophin Releasing Hormone ◽  
Testosterone Levels ◽  
Serum Lh ◽  
June July ◽  
Male Rhesus

Six male rhesus monkeys were kept under rigidly controlled conditions for 1–2 years. During August of the first year a thyrotrophin releasing hormone (TRH) test was performed on each of the monkeys by giving 10 μg TRH as a bolus injection. Significantly increased serum prolactin levels occurred 15 min after the injection. After a training period of 2 months, during which blood samples were collected every other day by puncture of the saphenous vein, blood was collected three times a week for 14 months. Serum levels of prolactin, LH, FSH and testosterone were measured by radioimmunoassay. Mean serum prolactin levels increased significantly during June, July and August in all six animals. Peak levels were observed in August and September and then levels declined gradually to reach a minimum in April and May. Mean serum testosterone levels closely paralleled the annual pattern of prolactin. Mean serum LH levels significantly decreased during the time when mean serum prolactin and testosterone levels were increasing and they increased again at the time of decreasing mean prolactin levels, i.e. mean serum LH and prolactin were negatively correlated. In individual monkeys, however, a rigid negative correlation between serum prolactin and LH could not be demonstrated. Mean serum FSH levels did not change significantly.

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