Altered Ovulation Pattern in Experimental Diabetes

Heat shock protein production and immunity and altered fetal development in diabetic pregnant rats

“…Diabetes mellitus comprises a group of metabolic diseases characterized by chronic hyperglycemia resulting from defects in insulin secretion, insulin action, or both (American Diabetes Association 2011). Impaired reproductive performance is a well-known result of the diabetic syndrome in many mammalian species, including humans (Chieri et al 1969;Kirchick et al 1978;Vomachka and Johnson 1982;Garris et al 1986). Placental dysfunction contributes to an increased frequency of fetal complications in diabetic pregnancies (Daskalakis et al 2008).…”

Deficits in Pituitary and Brain Cell Nuclear Retention of (³H)Estradiol in Diabetic Rats Deprived of Insulin: Time Course and Metabolic Correlates

“…Fat content of the diet has no ef fect on brain or pituitary estradiol uptake in diabetic animals deprived of insulin for 36 h. Circulating levels of triglyce rides, ketones, glucose, glycerol and free fatty acids were found to predict uptake levels to a significant extent, but no single metabolite is reliably predictive across tissues. These data demonstrate that insulin-dependent changes in brain and pitui tary uptake of estradiol in rats are slow to develop, and they support the hypothesis that at least some of the reproductive dysfunctions observed in diabetic rats may be the result of impaired cell nuclear estradiol binding in hypothalamus and pi tuitary.Impairment of reproductive function and performance is associated with diabetes mellitus in both human beings and animals [4,5,9,14,15,26]. In rats, this impairment in cludes disruption of normal estrous cycles [5,9,14,15] de layed sexual maturity [14], decreased numbers of ova shed when ovulation does occur [4], high rates of fetal resorption [5,14], diminished lactational performance [14] and reduc tions in ovarian and uterine weights [8,9,14], Reduced uter ine weights in diabetics are consistent with impaired ovari an steroidogenesis.…”

“…In rats, this impairment in cludes disruption of normal estrous cycles [5,9,14,15] de layed sexual maturity [14], decreased numbers of ova shed when ovulation does occur [4], high rates of fetal resorption [5,14], diminished lactational performance [14] and reduc tions in ovarian and uterine weights [8,9,14], Reduced uter ine weights in diabetics are consistent with impaired ovari an steroidogenesis. The ovaries of alloxan-diabetic rats dis play a diminished responsiveness to exogenously adminis tered gonadotropins, but endogenous gonadotropin levels seem to be normal [8,13,16].…”

Estrous Behavior and Pituitary and Brain Cell Nuclear Retention of [³Η]Estradiol in Chronically Insulin-Deficient Female Rats

“…Plasma glucose levels are significantly correlated with estradiol uptake levels in brain and pituitary, and with plasma radioactivity levels. These data support the hypothesis that some of the reproductive dysfunctions manifest in female diabetic rats are the result of alterations in nu clear binding of estradiol by central nervous tissue, and that chronic fuel deprivation may represent an important correlate of disruptions in normal steroid action among diabetics.A number of reproductive dysfunctions including failure to ovulate normally, conceive, or maintain pregnancy, are associated with diabetes mellitus in both animals and hu man beings [2,3,5,8,9,14]. Previous research has implicat ed the central nervous system as one of the possible sites of functional disruption, with the demonstration that acute in sulin deficiency leads to reduced estradiol uptake in hypothalamus-preoptic area and pituitary gland [4,7], re duction of cell nuclear estrogen receptor levels in hypothalamus-preoptic area [13], and reduction in lordosis behavior 17.13], Although shifts in plasma constituents reflect rapid met abolic responses to insulin deprivation, deficits in brain up take of estradiol develop relatively slowly in rats.…”