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 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.

Characterization of the inhibitory roles of RFRP3, the mammalian ortholog of GnIH, in the control of gonadotropin secretion in the rat: in vivo and in vitro studies

2010 ◽  
Vol 299 (1) ◽  
pp. E39-E46 ◽  
Author(s):  
R. Pineda ◽  
D. Garcia-Galiano ◽  
M. A. Sanchez-Garrido ◽  
M. Romero ◽  
F. Ruiz-Pino ◽  
...  
Keyword(s):  
Inhibitory Effect ◽  
Female Rats ◽  
Male Rats ◽  
High Dose ◽  
Gonadotropin Secretion ◽  
Male And Female Rats ◽  
Sites Of Action ◽  
Lh Secretion

RF-amide related peptides (RFRP), as putative mammalian orthologs of the avian gonadotropin-inhibitory hormone (GnIH), have been proposed as key regulators of gonadotropin secretion in higher vertebrates. Yet considerable debate has arisen recently on their physiological relevance and potential mechanisms and sites of action. Present studies were undertaken to further characterize the effects of RFRP on LH and FSH secretion by a combination of in vivo and in vitro approaches in male and female rats. Initial screening via intracerebroventricular (icv) administration of different analogs of RFRP1 (RFRP1–12 and RFRP1–20) and RFRP3 (RFRP3–8 and RFRP3–17), as well as the related neuropeptide FF (NPFF8), to gonadectomized (GNX) female rats evidenced significant, albeit modest, inhibitory effects on LH secretion only for RFRP3–8 and RFRP3–17, which were detectable at the high dose rage (1 nmol for RFRP3–8, 5 nmol for RFRP3–17). This moderate inhibitory action was also documented after icv administration of RFRP3–8 to intact and GNX male rats. In addition, systemic (intravenous) administration of RFRP3–8 decreased the circulating levels of both gonadotropins in GNX male rats. Likewise, RFRP3–8 inhibited basal and GnRH-stimulated LH secretion by pituitaries from GNX males in vitro. This inhibitory effect was blocked by the antagonist of RFRP receptors, RF9. In summary, our results support a putative inhibitory role of RFRP3 as ortholog of GnIH in the regulation of gonadotropin secretion in mammals, which appears to involve direct pituitary actions as well as potential central (hypothalamic) effects.

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.

scholarly journals Sex-specific vascular responses of the rat aorta: effects of moderate term (intermediate stage) streptozotocin-induced diabetes

2016 ◽  
Vol 94 (4) ◽  
pp. 408-415 ◽  
Author(s):  
Xiaoyuan Han ◽  
Sonali Shaligram ◽  
Rui Zhang ◽  
Leigh Anderson ◽  
Roshanak Rahimian
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Mrna Expression ◽  
Intermediate Stage ◽  
Diabetic Rats ◽  
Female Rats ◽  
Diabetic Rat ◽  
Male And Female ◽  
Male And Female Rats ◽  
Oxide Synthase

Hyperglycemia affects male and female vascular beds differently. We have previously shown that 1 week after the induction of diabetes with streptozotocin (STZ), male and female rats exhibit differences in aortic endothelial function. To examine this phenomenon further, aortic responses were studied in male and female rats 8 weeks after the induction of diabetes (intermediate stage). Endothelium-dependent vasodilation (EDV) to acetylcholine (ACh) was measured in phenylephrine (PE) pre-contracted rat aortic rings. Concentration response curves to PE were generated before and after L-NAME, a nitric oxide synthase (NOS) inhibitor. Furthermore, mRNA expression of endothelial nitric oxide synthase (eNOS) and NADPH oxidase subunit (Nox1) were determined. At 8 weeks, diabetes impaired EDV to a greater extent in female than male aortae. Furthermore, the responsiveness to PE was significantly enhanced only in female diabetic rats, and basal NO, as indicated by the potentiation of the response to PE after L-NAME, was reduced in female diabetic rat aortae to the same levels as in males. In addition, eNOS mRNA expression was decreased, while the Nox1 expression was significantly enhanced in diabetic female rats. These results suggest that aortic function in female diabetic rats after 8 weeks exhibits a more prominent impairment and that NO may be involved.

Postreceptor defect in insulin action in streptozotocin-induced diabetic rats

1989 ◽  
Vol 256 (5) ◽  
pp. E624-E630 ◽  
Author(s):  
H. Nishimura ◽  
H. Kuzuya ◽  
M. Okamoto ◽  
K. Yamada ◽  
A. Kosaki ◽  
...  
Keyword(s):  
Glucose Transporter ◽  
Insulin Dose ◽  
Insulin Binding ◽  
Diabetic Rats ◽  
Glucose Disposal ◽  
Maximal Response ◽  
Metabolic Clearance ◽  
Glucose Clamp Technique

To clarify the mechanism(s) responsible for the insulin resistance in streptozotocin (STZ)-treated diabetic rats, we studied insulin-induced glucose disposal by using the glucose clamp technique and measured insulin receptor and glucose transporter of muscles. The insulin dose-response curve of the metabolic clearance rate (MCR) of glucose revealed a decrease of the maximal response without a rightward shift in STZ rats. Maximal MCR was even lower when clamped at 300 rather than 150 mg/dl of blood glucose levels. Insulin binding to the crude plasma membrane of muscles from STZ rats was increased compared with controls. The number of glucose transporter of the plasma and microsomal membranes were significantly decreased in STZ rats. These in vivo and in vitro studies using skeletal muscles suggest that in STZ-treated diabetic rats 1) a defect or defects exist in the signal transduction mechanism of insulin in postbinding steps, 2) the decreased maximal MCR is related at least partly to the decrease of glucose transporter numbers, and 3) a defect in glucose metabolism (postglucose transport defect) is also present.

Abstract 17462: Relevance of Regulatory T Cells to Gender Dimorphism in Pulmonary Hypertension

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Rasa Tamosiuniene ◽  
Linh Nguyen ◽  
Ayala Luria ◽  
Joshua Sante ◽  
Toshie Saito ◽  
...  
Keyword(s):  
T Cell ◽  
Vascular Wall ◽  
Reciprocal Relationship ◽  
Female Rats ◽  
Gender Dimorphism ◽  
Control Male ◽  
Control Female ◽  
Male And Female Rats ◽  
Endogenous Estrogen

Idiopathic Pulmonary Arterial Hypertension (IPAH) is a disease with female predominance. A growing body of evidence shows reciprocal relationship between sex steroids and the immune system. The aim of the present study was to determine whether the absence of Tregs with the presence of endogenous estrogen mediate the development of PH in a gender-specific manner and if protective signaling pathways of Tregs prevent gender dimorphism of PH susceptibility in T cell deficient animal model of PH. Methods and Results: in two utilized models of PH inbred Wag T cell deficient athymic (AT) nude male and female rats were given s/c SU5416 in normoxia or treated with chronic hypoxia (CH) for 21d. In IR experiments, AT rats received purified CD4+CD25+hi/Tregs. We also tested the effect of murine/human Tregs or CD4+CD25- on primary rat lung, cardiac and human lung microvascular ECs (RLMECs, HLMECs, RCMECs) with set-up of cocultures. In both PH models treatment resulted in development of PH with significantly higher RVSP and particular significantly pronounced RVH in female than in male in both SU5416 and CH groups (Fulton index: 0.41±0.01vs.0.33±0.02 and 0.52±0.03vs.0.37±0.01, p< 0.05). However, circulating estrogen levels were found to be significantly elevated in female than in male in all animal groups. For both female and male AT animals IR of Tregs prevented PH with RV remodeling, as well as decreased perivascular fibrosis and increased estrogen receptor (ER)β expression in lung and RV vascular wall. In vitro studies on coculture of Tregs with RLMECs and RCMECs resulted in an upregulation of IL-10, HO-1, PDL1, ERα, ERβ, activation of pAKT pathway, and endothelial nitric oxide synthase (eNOS), which was abrogated with ER antagonist ICI182,780. In addition, compared with control male AT rats, control female animals had increased expression of HO1, HO2 enzymes in lung and RV vascular wall endothelial/Reca+ cells as well as increased capillary density in RV. Thus, differential HO expression between the genders might account for the PH susceptibility. Conclusions: Our data suggest that Tregs signaling is required as a major mechanism with possible mutual interaction of endogenous estrogen to prevent endothelial injury related gender dimorphism for the development of PH.

scholarly journals 5-HT1 and 5-HT2 receptor activation reduces N-methyl-D-aspartate (NMDA)-stimulated LH secretion in prepubertal male and female rats

2003 ◽  
pp. 121-127 ◽  
Author(s):  
L Pinilla ◽  
LC Gonzalez ◽  
M Tena-Sempere ◽  
E Aguilar
Keyword(s):  
Methyl Ester ◽  
Receptor Activation ◽  
Female Rats ◽  
Receptor Subtypes ◽  
Serotoninergic System ◽  
Gonadotropin Secretion ◽  
Male And Female ◽  
Receptor Agonists ◽  
Male And Female Rats ◽  
Lh Secretion

OBJECTIVE: Excitatory amino acids and serotonin are involved in the control of gonadotropin secretion. The actions of these neurotransmitters are interconnected and recently we have reported that 5-HT(1) and 5-HT(2) receptor agonists blunted (+/-)-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA)-stimulated GH secretion in prepubertal rats. The present experiments were carried out to analyze the effects of activation of different 5-hydroxytryptamine (5-HT) receptor subtypes on gonadotropin secretion and their role in the N-methyl-d-aspartate (NMDA)-stimulated LH release. DESIGN AND METHODS: We analyzed the gonadotropin secretion after manipulation of serotoninergic and aminoacidergic systems and their interactions in 5-, 16- and 23-day-old male and female rats. To this end, serum LH and FSH concentrations were measured in rats treated with 5-hydroxytryptophan methyl ester (5-HTP) (a precursor of 5-HT synthesis) plus Fluoxetine (Fx, a blocker of 5-HT reuptake), d,l-p-chlorophenyl-alanine methyl ester (PCPA, a blocker of 5-HT synthesis), R-(+)-8-hydroxydipropylaminotetralin hydrobromide (8-OH-DPAT, an agonist of 5-HT(1A) receptors), (+/-)-2,5-dimethoxy-4-iodoamphetamine hydrochloride (DOI) and alpha-methyl-5-hydroxytryptamine (alpha-Me-5-HT, agonists of 5-HT(2) receptors), and 1-Phenylbiguanide (1-PHE an agonist of 5-HT(3) receptors). In addition, the effects of 8-OH-DPAT and DOI on NMDA-stimulated LH secretion were analyzed. RESULTS: Neither the activation nor blockade of the serotoninergic system modified LH secretion. Basal gonadotropin secretion remained unchanged in 23-day-old male and female rats after activation of 5-HT(1A), 5-HT(2) and 5-HT(3) receptors. The stimulatory effect of NMDA on LH secretion was blocked in both sexes after activation of the serotoninergic system, through specific 5-HT(1) and 5-HT(2) receptor agonists. CONCLUSIONS: Activation of serotoninergic receptors decreased the stimulatory effect of NMDA on LH secretion in prepubertal male and female rats.

REGULATION OF THE METABOLISM OF PITUITARY NUCLEIC ACIDS IN FEMALE RATS

1980 ◽  
Vol 85 (1) ◽  
pp. 1-8 ◽  
Author(s):  
J. BÍRÓ
Keyword(s):  
Nucleic Acids ◽  
Intraperitoneal Injection ◽  
Anterior Pituitary ◽  
Rna Metabolism ◽  
Female Rats ◽  
Biphasic Effect ◽  
Lh Rh ◽  
Lh Releasing Hormone

SUMMARY Ovariectomy caused an increase in the metabolism of pituitary nucleic acids. This effect was reversed in vivo by a biphasic action of oestradiol-17β which first facilitated RNA metabolism after 8 h and then inhibited it 16 h after intraperitoneal injection. To analyse the origin of this biphasic effect the roles of LH releasing hormone (LH-RH) and hysterectomy were examined. Incorporation of uridine into the RNA of the anterior pituitary gland of female rats was inhibited both in vivo and in vitro by LH-RH. Hysterectomy augmented the increase in the RNA metabolism caused by ovariectomy whereas steroid-free uterine extracts inhibited the increase significantly. We have concluded that extrapituitary factors may be involved in the effects of oestrogen on the metabolism of pituitary nucleic acids.

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