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目的探讨孕鼠肥胖对雌性子代大鼠发生多囊卵巢综合征(PCOS)的影响和可能机制。方法子代实验组为高能饲料喂养诱导的肥胖妊娠期大鼠与正常雄性大鼠合笼后出生的雌性仔鼠,子代对照组为普通的饲料喂养的雌性大鼠与正常雄性大鼠合笼后出生的雌性仔鼠。两组雌性仔鼠(子代对照组17只,子代实验组19只)生长至14~16周处死,取卵巢组织观察两组仔鼠卵巢大体形态并进行HE染色,取静脉血检测大鼠血清睾酮、胰岛素、空腹血糖和血脂水平。蛋白印记检测卵巢组织ERK1和ERK2的表达。结果高脂喂养3周后,母代实验组体重明显大于母代对照组(P<0.05);子代实验组卵巢呈多囊性改变,子代实验组血糖和雄激素均高于子代对照组(P<0.05)。与子代对照组相比,子代实验组ERK1和ERK2的表达均升高(P<0.05)。结论母鼠妊娠期肥胖可能是子代成年期发生PCOS的一个高风险因素。
Objective To investigate the effects of obesity in pregnant rats on the development of polycystic ovary syndrome (PCOS) in female offspring rats and its possible mechanism. Methods The offspring of experimental group were fed with high-energy feed-induced obese pregnant rats and normal male rats were born after the female offspring, the offspring of the control group of normal feed-fed female rats and normal male rats cage Postnatal female offspring. Two groups of female offspring (17 offspring in control group and 19 offspring in experimental group) were sacrificed and were sacrificed 14 to 16 weeks later. The ovaries of the two groups were observed for ovary morphology and HE staining. Serum testosterone, insulin, fasting blood glucose and lipid levels. Western blot was used to detect the expression of ERK1 and ERK2 in ovarian tissue. Results After 3 weeks of high-fat diet, the body weight of the experimental group was significantly higher than that of the parental control group (P <0.05). The ovary of the progeny group showed polycystic changes, while the blood glucose and androgen levels in the progeny experimental group were higher than those in the progeny control group (P <0.05). Compared with the offspring control group, the expression of ERK1 and ERK2 in offspring experimental group were increased (P <0.05). Conclusion The maternal obesity in pregnancy may be a high risk factor of PCOS in offspring adulthood.