scholarly journals Analysis of hypothalamo-hypophyseo-gonadal relationships in female rats with experimental diabetes

1994 ◽  
Vol 40 (1) ◽  
pp. 46-50 ◽  
Author(s):  
V N Babichev ◽  
Ye L Adamskaya ◽  
T A Peryshkova
Keyword(s):  
Nuclear Receptors ◽  
Sex Hormones ◽  
Experimental Diabetes ◽  
Streptozotocin Diabetes ◽  
Female Rats ◽  
Gonadotropin Secretion ◽  
Estral Cycle ◽  
Lh Rh ◽  
Reduced Activity ◽  
Intact Rats

Hypothalamo-hypophyseo-gonadal system functional activity was studied in rats with streptozotocin diabetes. In intact rats concentrations of sex hormones nuclear receptors were measured in the hypothalamic preopticoanterior, mediobasal segments and in the adenohypophysis, as were blood serum gonadotropins and sex hormones. Estradiol and progesterone were injected to ovariectomized females and LH-RH levels measured in preopticoanterior segment of the hypothalamus, arcuate nucleus, and median eminence, as well as LH and FSH concentrations in the blood in order to detect disorders in basal and cyclic gonadotropin secretion. Streptozotocin injection to cycling females disordered the estral cycle and was associated with reduction of LH, FSH, and sex hormones basal and cyclic secretion. Estradiol nuclear receptors concentrations reduced in the preopticoanterior hypothalamus and hypophysis, the count of nuclear testosterone-binding sites reduced only in the hypophysis. Gonadotropin wave stimulated with sex steroids in ovariectomized females was reduced in diabetes because of changed activity of LH-RH-producing system. We believe that changes in basal and cyclic secretion of gonadotropins in rat females with experimental diabetes is explained by reduced activity of LH-RH-producing system and receptor binding at the level of the hypothalamo-hypophyseal complex.

scholarly journals Basal and LH-RH-stimulated gonadotropin secretion in oophorectomized female rats with streptozotocin-induced diabetes

1994 ◽  
Vol 40 (1) ◽  
pp. 43-46 ◽  
Author(s):  
V N Babichev ◽  
Ye L Adamskaya ◽  
T A Peryshkova
Keyword(s):  
Hormone Therapy ◽  
Reproductive System ◽  
Experimental Diabetes ◽  
Streptozotocin Diabetes ◽  
Female Rats ◽  
Gonadotropin Secretion ◽  
Insulin Effect ◽  
Streptozotocin Induced Diabetes ◽  
Lh Rh

In vitro insulin effect on basal and LH-RH- stimulated gonadotropin secretion in oophorectomized female rats with streptozotocin diabetes administered estradiol as replacing hormone therapy was studied. The results were compared to those obtained after a similar incubation of adenohypophyses of oophorectomized rats and of oophorectomized rats administered estradiol. Estradiol was found to change the type of LH-RH-stimulated gonadotropin secretion in oophorectomized animals. Basal, but not LH-RH-stimulated gonadotropin secretion, was increased in rats with experimental diabetes as against other groups. Insulin inhibited basal and increased LH-RH-stimulated gonadotropin secretion in oophorectomized rat’s with streptozotocin diabetes administered estradiol. A conclusion is made about impaired sensitivity of hypophyseal gonadotrophs to LH-RH in streptozotocin diabetes and about a possible contribution of insulin to regulation of body reproductive system at the level of hypophysis.

scholarly journals Neuroendocrine control of the pituitary gonadotropic function in experimental diabetes

2019 ◽  
Vol 43 (3) ◽  
pp. 43-47
Author(s):  
V. N. Babichev ◽  
E. I. Adamskaya ◽  
T. A. Kuznetsova ◽  
I. V. Shishkina
Keyword(s):  
Nuclear Receptors ◽  
Experimental Diabetes ◽  
Diabetic Rats ◽  
Female Rats ◽  
Maximal Response ◽  
Basal Secretion ◽  
Male And Female Rats ◽  
Lh Rh ◽  
Lh Secretion

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.

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
Keyword(s):  
Nuclear Receptors ◽  
Negative Feedback ◽  
Reproductive Function ◽  
Male Rats ◽  
Maximal Response ◽  
Gonadotropin Secretion ◽  
Releasing Hormone ◽  
Lh Rh ◽  
Lh Releasing Hormone

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.

THE HYPOTHALAMUS AND PROPYLTHIOURACIL-INDUCED GOITRE IN THE RAT

1963 ◽  
Vol 42 (2) ◽  
pp. 254-262 ◽  
Author(s):  
J. J. van der Werff ten Bosch ◽  
H. E. Swanson
Keyword(s):  
Steady State ◽  
Thyroid Hormone ◽  
Adult Female ◽  
Normal Diet ◽  
Anterior Hypothalamus ◽  
Female Rats ◽  
Intact Rats

ABSTRACT Adult female rats were given a normal diet, or a diet which contained 0.15% propylthiouracil. At the beginning of the experiment one half of the rats were left intact, whilst the others received an electrolytic basal midline lesion in the anterior hypothalamus. Of each of the four groups of rats, one half was killed after 14 days, the others after 28 days. It was found (both after 14 and after 28 days) that the presence of a lesion reduced the thyroid weight to approximately 75% of the value in intact rats on the same diet, which might be normal or contain propylthiouracil. Propylthiouracil caused thyroid enlargement (to 278% after 14 days and 352–360% after 28 days) in intact rats as compared with intact rats on a normal diet, and in lesioned rats as compared with lesioned rats on a normal diet. It is concluded that lesions cause a lowered steady state of the thyroid-pituitary feed-back system, but that this system responds normally to the alteration of the steady state caused by the propylthiouracil-induced block in thyroid hormone output.

scholarly journals Sex Hormones Regulate Hepatic Fetuin Expression in Male and Female Rats

2014 ◽  
Vol 34 (2) ◽  
pp. 554-564 ◽  
Author(s):  
Sang Woo Kim ◽  
Jung-Won Choi ◽  
Dong Seok Lee ◽  
Jong Won Yun
Keyword(s):  
Sex Hormones ◽  
Female Rats ◽  
Male And Female ◽  
Male And Female Rats

Desensitization of gonadotropin responses to kisspeptin in the female rat: analyses of LH and FSH secretion at different developmental and metabolic states

2008 ◽  
Vol 294 (6) ◽  
pp. E1088-E1096 ◽  
Author(s):  
J. Roa ◽  
E. Vigo ◽  
D. García-Galiano ◽  
J. M. Castellano ◽  
V. M. Navarro ◽  
...  
Keyword(s):  
Current Data ◽  
Female Rats ◽  
Pharmacological Intervention ◽  
Female Rat ◽  
Continuous Administration ◽  
Gonadotropin Secretion ◽  
Dynamic Regulation ◽  
Intracerebral Administration ◽  
Metabolic States ◽  
Transient Elevation

Kisspeptins have emerged as potent elicitors of gonadotropin secretion and, therefore, putative targets for pharmacological intervention. In this context, desensitization of gonadotropin responses to continuous administration of kisspeptins has begun to be characterized, but information so far available is mostly restricted to LH responses in males, whereas the similar phenomenon in females, of obvious therapeutic interest, remains virtually unexplored. We report herein LH and FSH responses to continuous intracerebral administration of kisspeptin in female rats at different developmental and metabolic states. Infusion of kisspeptin-10 to adult female rats induced a transient elevation in serum LH concentrations, followed by a precipitous drop and normalization of LH levels thereafter. Elevation of LH after kisspeptin infusion was prolonged in underfed animals; a phenomenon mimicked by leptin administration. Conversely, FSH levels were persistently heightened along continuous kisspeptin infusion, but duration of this response was shortened by undernutrition. In pubertal females, LH and FSH levels remained elevated at the end of a 7-day infusion of kisspeptin; responses whose magnitude was augmented by subnutrition but not mimicked by leptin. In all settings, terminal gonadotropin-releasing hormone responses were fully preserved, suggesting that eventual desensitization must occur upstream from the pituitary. In summary, our current data document the pharmacological consequences of continuous administration of kisspeptin to female rats, with remarkable differences being detected between LH and FSH responses, in different developmental and metabolic states. These observations of potential pharmacological interest might help also to delineate the physiological roles of kisspeptins in the dynamic regulation of gonadotropin secretion in the female.

Abstract P136: Effects Of Sex Hormones On The Hemodynamic And Sympathetic Responses To Centrally Administered Tumor Necrosis Factor-α In Rats

Hypertension ◽  
2020 ◽  
Vol 76 (Suppl_1) ◽  
Author(s):  
Yiling Cao ◽  
Baojian Xue ◽  
Yang Yu ◽  
Alan K Johnson ◽  
Shun-Guang Wei
Keyword(s):  
Heart Failure ◽  
Tumor Necrosis Factor ◽  
Sex Hormones ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Female Rats ◽  
Tnf Α ◽  
Sympathetic Responses ◽  
Factor Α ◽  
Necrosis Factor

Inflammation plays an important role in the pathophysiology of cardiovascular dysfunction and neurohumoral excitation in heart failure and hypertension. Growing evidence has demonstrated significant sex differences in the inflammatory response and immune processes, with estrogen exerting an anti-inflammatory effects and testosterone potentially having pro-inflammatory influence. We previously reported that central administration of tumor necrosis factor-α (TNF-α) elicited different effects on blood pressure (BP), heart rate (HR) and renal sympathetic nerve activity (RSNA) in male and female rats. Whether the sex steroids estrogen and testosterone contribute to the observed differences in TNF-α-induced hemodynamic and sympathetic responses remains unknown. We hypothesized that estrogen protects against TNF-α-induced sympathetic excitation and pressor responses while testosterone enhances these excitatory outcomes in response to TNF-α. Female or male Sprague Dawley rats (10-12 weeks) anesthetized with ketamine plus xylazine underwent bilateral ovariectomy or castration, respectively, 2 weeks prior to study. Sham-operated (Sham) female or male animals served as controls. TNF-α (100 ng) was administered intracerebroventricularly (ICV). BP (mmHg), HR (bpm) and RSNA (% change) were recorded in urethane anesthetized rats. In ovariectomized female rats (n=6), ICV TNF-α induced significantly (*p<0.05 vs. Sham) larger increases in BP (19.3 ± 1.4* vs. 12.8 ± 1.2 ), HR (76.3 ± 4.8* vs. 51.5 ± 4.3) and RSNA (104.8 ± 6.9* vs. 72.4 ± 5.1), compared with Sham-female rats, that began within 20-30 mins and peaked at 90-120 mins after ICV injection. In castrated male rats (n=6), ICV TNF-α-elicited significantly smaller increases in BP (15.2 ± 1.3* vs. 21.8 ± 1.6), HR (57.7 ± 4.2* vs. 82.6 ± 4.1) and RSNA (72.6 ± 4.3* vs. 110.3 ± 4.7), compared with Sham-male animals. These data indicate a distinct role of sex hormones estrogen and testosterone in central inflammation-driven cardiovascular and sympathetic activation and suggest a protective effect of estrogen and a harmful effect of testosterone in the development of hypertension and heart failure.

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