Study Of Insulin Resistance And Fertility Function On Female Rats With Fetal Growth Retardation

Objective To explore the influences of fetal growth retardation (FGR) andinsulin resistance at their adult stage on ovarian development, function andglucose metabolism in female rats. Methods FGR models were constructed byligating uterine artery of pregnant rats. The Sprague-Dawley(SD) pregnant ratson day17of gestation were divided into experimental group (n=14)performingbilateral uterine artery ligation (UAL) and control group (n=8)performing sham operation. Thirty newborn female rats were chosen from FGRgrope and control group respectively, and they were divided into two groups andprovided with normal diet. Fasting plasma glucose(FPG), and fastinginsulin(FINS) of FGR group and control group were detected, and glucosetolerance and hyperinsulinemic-euglycemic clamp test was processed tocalculate glucose intake rate (GIR). Isletβ-cell endocrine function and insulinsensitivity in peripheral tissue were evaluated. The change of oestrous cycle andtestosterone level were observed in both groups. The ovarian tissues of bothgroups were evaluated, and Western blot and immunohistochemistry were usedto measure the content and expressions of GSK-3β/p-GSK-3β/GLUT4.Results FPG and insulin level of adult FGR rats were5.6±0.82mmol/L and59.06±14.00mU/L respectively，which were significantly higher than those of rats in control group(4.55±0.57mmol/L and47.20±15.00mU/Lrespectively，t was-3.353and2.203, both P <0.05). GIR in experimentalgroup was7.95±0.8mg/kg· min, which was lower than that12.99±0.35mg/kg·min in control group (P<0.05). Compared with that of controlgroups, the estrous cycle of FGR rats prolonged significantly, and testosteronelevel rose. The estrous cycle of FGR group (8.3±1.5days) was longer than thatof control group (5.1±0.9days). Ovarian follicle of various stages and corepusluteum were found in ovary of two groups, but the differences in ovarianmorphology and weight were not significant. The expression of GSK-3β inFGR rats elevated significantly, but the expression of p-GSK-3β descended, incontrary, Under the stimulation of insulin the expression of GLUT4in FGRgroup‘s ovarian degrade significantly. Conclusion (1) FGR models wereconstructed by ligating uterine artery of pregnant rats.(2) Insulin resistance inadult stage exists in FGR female rats.(3) Prolonging estrous cycle andoligo-ovulation might occur in female FGR rats. Meanwhile, testosterone leveland insulin level elevate.(4)Abnormal glucose metabolism resemblingpolycystic ovary syndrome may occur in FGR rats. Metabolic dysfunction in theFGR group has close relationship with whole body condition, which defectiveinsulin signal within ovaries.