scholarly journals The hypophyseogonadal system of male rats with diabetes: an experimental study

1993 ◽  
Vol 39 (1) ◽  
pp. 42-45 ◽  
Author(s):  
V. N. Babichev ◽  
T. A. Peryshkova ◽  
Ye. I. Adamskaya

The hypophyseogonadal system of male rats with streptozotocin-induced diabetes was studied. The hypophyseal sensitivity to LH releasing hormone was analyzed in vitro and concentrations of sex hormone nuclear receptors in the adenohypophysis, participating in gonadotropin secretion regulation according to a negative feedback mechanism, measured. Streptozotocin injection reduced blood testosterone concentration and levels of androgen nuclear receptors in the rat hypophysis. Blood LH and FSH levels in the rats with diabetes were virtually the same as in intact animals. In vitro experiments have demonstrated that diabetes development in rats did not influence the level of LH basal secretion by the hypophysis. The maximal response to LH releasing hormone was recorded in the control males in 3h incubation, whereas the rate of LH secretion in the experimental animals did not differ from the normal one. The authors suggest that changed mechanism of the hypothalamo-hypophyseo-gonadal system regulation in experimental diabetes is related to the hypophyseal disorders, involving reduction of the LH-RH-stimulated gonadotropin release and of the testosterone receptor levels, this resulting in poor reproductive function control according to the negative feedback principle.

1977 ◽  
Vol 73 (2) ◽  
pp. 309-319 ◽  
Author(s):  
J. DULLAART

SUMMARY Pituitary glands from immature female and male rats aged between 5 and 30 days were incubated in vitro and the effect of LH releasing hormone (RH) on the release of LH and FSH was studied. Pituitary gonadotrophin contents were also measured. Gonadotrophin release showed changes with age as well as sex differences: after LH-RH stimulation the female pattern of release of LH and FSH (expressed per mg pituitary tissue) showed a peak at day 15; the male pattern of LH release was characterized by a steady increase with age, whereas FSH release stayed more or less constant from day 10 onwards. In both sexes the LH:FSH ratio increased with age, both in pituitary gonadotrophin content and in the mixture of gonadotrophins released. It is discussed, that the prepubertal development of pituitary gonadotrophic function might be determined on the one hand by rather autonomous growth processes (more or less similar in female and male hypophyses) and on the other hand by modulating influences of sex steroid hormones, which are different in female and male animals.


2019 ◽  
Vol 43 (3) ◽  
pp. 43-47
Author(s):  
V. N. Babichev ◽  
E. I. Adamskaya ◽  
T. A. Kuznetsova ◽  
I. V. Shishkina

The hypothalamo-pituitary-gonadal system was examined in male and female rats with experimental diabetes in­duced by streptozotocin (STZ). Injection of STZ caused a decrease of testosterone (T) concentration and of T nuclear receptors in the pituitary. The levels of luteinizing and follicle stimulating hor­mones (LH and FSH) in the blood of diabetic rats did not differ from those in intact animals. In vitro experiments showed that the development of diabetes did not change the basal secretion of LH by the pituitary in males. Maximal response to LH-RH was record­ed in control males after 3-hour incubation, whereas the rate of LH secretion in experimental rats did not differ from basal values. In­jection of STZ to cycling females disordered the estrous cycle and involved decreases of the basal and cyclic secretion of LH, FSH, and sex hormones. The concentrations of estradiol nuclear receptors in the preoptic anterohypothalamic region and pituitary decreased, whereas the number of T-binding sites decreased only in the pitui­tary. Sex hormone-stimulated gonadotropin wave in oophorect- omized females was decreased in diabetes, which was due to changed activity of the LH-RH producing system. The authors hy­pothesize that changes in the mechanism of regulation of the hy­pothalamo-pituitary-gonadal system in experimental diabetes are re­lated to pituitary disorders in males, whereas changed basal and cy­clic secretion of LH and FSH in females is caused by disordered activity of the LH-RH production and receptor binding at the level of the hypothalamo-pituitary complex.


1986 ◽  
Vol 111 (2) ◽  
pp. 309-315 ◽  
Author(s):  
M. L. Vitale ◽  
M. N. Parisi ◽  
S. R. Chiocchio ◽  
J. H. Tramezzani

ABSTRACT The effects of serotonin (5-HT) on the release of gonadotrophins and LH-releasing hormone (LHRH) were examined in an in-vitro perifusion system using median eminences and/or anterior pituitaries obtained from male or pro-oestrous female rats. Animals were killed by decapitation between 12.00 and 13.00 h. A serial double-chamber perifusion system was employed. Three types of experiments were performed. In the first, median eminences were placed in the first chamber and one anterior pituitary in the second chamber. In the second group, only the anterior pituitary was perifused. In the third group, only five median eminences were perifused. In the first and second experiments, LH, FSH and prolactin were determined in the perifusion efflux by radioimmunoassay (RIA). In the third experiment, LHRH was determined by RIA. Addition of 5-HT (final concentrations 0·06, 0·6 and 6·0μmol/l) into the first chamber containing the median eminences stimulated the release of LH and FSH from the pituitary, but did not affect the levels of prolactin in the effluent in the same experiment (prooestrous rats). The stimulatory effect of 5-HT was blocked by the addition of cyproheptadine (1 μmol/l) in the perifusion fluid. The introduction of 5-HT (0·6 μmol/l) into the tube connecting the first and second chambers did not modify the release of LH, nor did 5-HT added to the pituitaries perifused alone. Injection of 5-HT into the first chamber (median eminences), containing tissue samples from male rats, stimulated LH release, but to a significantly (P< 0·001) lower degree than that found when samples from pro-oestrous females were used (P< 0·0001). When median eminences from pro-oestrous rats were perifused alone, injection of 5-HT produced an immediate release of LHRH which peaked during the first 10 min of collection and lasted for 30 min; in these experiments, a clear relationship existed between dose of 5-HT and release of LHRH (P<0·02). The stimulatory effect of 5-HT was blocked by the addition of cyproheptadine (5 μmol/l) or methiothepin (5 μmol/l). These results demonstrate that 5-HT stimulates gonadotrophin release by acting directly on LHRH terminals in the median eminence from pro-oestrous rats. Furthermore, the effect of 5-HT on LHRH release was dose dependent and was nullified by 5-HT receptor blockers (cyproheptadine and methiothepin). J. Endocr. (1986) 111, 309–315


Endocrinology ◽  
1972 ◽  
Vol 90 (6) ◽  
pp. 1578-1581 ◽  
Author(s):  
LUCIANO DEBELJUK ◽  
AKIRA ARIMURA ◽  
ANDREW V. SCHALLY

1992 ◽  
Vol 134 (2) ◽  
pp. 269-NP ◽  
Author(s):  
P. Garnelo ◽  
L. Pinilla ◽  
F. Gaytan ◽  
E. Aguilar

ABSTRACT Acute and long-term effects of neonatal and prepubertal treatments with an LH-releasing hormone agonist (LHRH-A) were studied in Wistar male rats. Animals injected with d-Ala6-d-Gly10-LHRH ethylamide (2 μg/kg per day) or vehicle from days 1 to 15 or from days 16 to 29 were killed at different ages. Treatment between days 1 and 15 induced a decrease in both pituitary FSH and LH content as well as a reduction in plasma FSH and blockade of the response to LHRH. These effects were apparent on day 16 after treatment. Basal and human chorionic gonadotrophin (hCG)-stimulated progesterone and testosterone secretion in vitro was similar in testes from male rats treated with LHRH-A or vehicle. Reduced testicular weight was observed until day 90, whereas puberty, spermatogenesis and fertility were unaffected. The decrease in plasma FSH concentrations after neonatal treatment with LHRH-A was also found in groups of animals killed on day 10 and was possibly the cause of reduced testicular weight, since treatment with FSH from day 1 to day 15 blocked the effect of LHRH-A. Likewise, treatment with LHRH-A from day 1 to day 15 also reduced FSH and LH secretion in males orchidectomized on day 1 of life. Animals injected with LHRH-A from day 15 to day 29 exhibited, at the end of the treatment period, reduced testicular weight, and decreased pituitary gonadotrophin content and plasma FSH concentrations, whereas LH plasma concentrations were normal. In adulthood, the pituitary-testis function did not vary from normal. Our results demonstrate that: (1) administration of LHRH-A from day 1 to day 15 of life desensitized the gonadotrophs, which in turn lowered plasma gonadotrophin concentrations and caused a long-term reduction in testis weight without changes in the quality of spermatogenesis or reproductive activity in adulthood; (2) chronic treatment with LHRH-A during the neonatal period did not result in a steroidogenic lesion; and (3) administration of LHRH-A from day 15 to day 29 produced only a transient reduction in testicular weight and in spermatogenesis. Journal of Endocrinology (1992) 134, 269–277


1981 ◽  
Vol 88 (1) ◽  
pp. 39-47 ◽  
Author(s):  
S. R. MILLIGAN ◽  
G. S. SARNA

Portacaval anastomosis (PCA) in the rat may be a useful experimental model for examining endocrine changes that occur during cirrhosis of the liver. A marked reduction in diet intake and body weight occurs in rats after establishing the shunt and studies were undertaken to determine the relationship of these effects to the testicular atrophy that also follows PCA. Control, sham-operated animals, experiencing a reduction in food intake similar to that of the animals with a PCA, showed reduced plasma levels of LH and testosterone but also exhibited a marked testicular response to LH. This was consistent with increased sensitivity of the hypothalamic-pituitary axis to the negative feedback of gonadal steroids in chronically underfed animals. Male rats with a PCA exhibited similarly reduced levels of LH and testosterone, but showed poor secretory responses of the pituitary gland to LH releasing hormone (LH-RH) and of the testis to LH. Testicular atrophy and cessation of spermatogenesis occurred in the animals with a PCA. These results suggested that the effects of PCA on the pituitary-gonadal axis cannot simply be explained as a consequence of the restricted intake of diet. This was confirmed by the responses to castration. In both fed and underfed sham-operated rats, castration resulted in a rapid and sustained increase in plasma LH and both groups showed a marked LH secretory response to LH-RH. In contrast, in animals with a PCA castration had little effect on plasma LH and the pituitary response to LH-RH was still poor. The effects of PCA cannot be simply explained by impeded metabolism of gonadal steroids causing increased negative feedback on the hypothalamic-pituitary axis.


1981 ◽  
Vol 90 (3) ◽  
pp. 345-354 ◽  
Author(s):  
KATHLEEN A. ELIAS ◽  
C. A. BLAKE

Changes at the anterior pituitary and/or hypothalamic levels which result in selective FSH release during late pro-oestrus in the cyclic rat were investigated. The possible involvement of decreasing serum concentrations of oestrogen during pro-oestrus in such changes was studied. Rats were decapitated at 12.00 h on pro-oestrus, before the onset of the LH surge and first phase of FSH release, or at 24.00 h on pro-oestrus, shortly after the onset of the second or selective phase of FSH release. Other rats were given oestrogen (OE2) at 14.00 h and killed at 24.00 h pro-oestrus. Paired hemi-anterior pituitary glands were incubated with vehicle or OE2 with or without synthetic LH-releasing hormone (LH-RH) or hypothalamic acid extracts prepared from rats killed at 12.00 or 24.00 h on pro-oestrus. At 24.00 h pro-oestrus, serum FSH concentration was high while serum LH concentration was low regardless of whether rats were given OE2. Glands collected and incubated at 24.00 h released more FSH and less LH than did glands collected and incubated at 12.00 h pro-oestrus. Administration of OE2 in vivo and/or in vitro did not affect these responses. The increments in LH and FSH release attributed to LH-RH or hypothalamic extracts in the glands incubated at 24.00 h were not different from those of the glands incubated at 12.00 h. Also, the hypothalamic extracts prepared from rats killed at 24.00 h were no more effective than the extracts prepared from rats killed at 12.00 h in releasing LH or FSH from glands incubated at 12.00 or 24.00 h pro-oestrus. Administration of OE2 in vivo caused a small suppression of LH-RH-induced FSH release. We suggest that a change occurs at the level of the anterior pituitary gland during the period of the LH surge and first phase of FSH release to increase basal FSH secretion selectively and cause, at least in part, the second phase of increased serum FSH. This change is not mediated by a decrease in serum oestrogen concentration. We failed to observe any evidence that LH-RH causes preferential FSH release during late pro-oestrus or that a hypothalamic peptide with a preferential FSH releasing ability is involved in FSH release at this time.


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