| Obesity popularity has grown with the improvement of living standards, meanwhilediseases are caused by obesity is growing fast. Obesity can lead to a variety of conditions, eachorgan in the body is likely to be affected, especially to women. In the the reproductive system,obesity can lead to infertility rates rise results from ovulation disorder, polycystic ovarysyndrome (PCOS), early preeclampsia, gestational hypertension, menstrual disorders,gynecologic cancer.Apolipoprotein e (ApoE) is a member of the Apolipoprotein family. ApoE synthesis mainlyin the liver and the brain, macrophages can also be part of synthesis. The function of ApoEinclude involved in the repair of the nervous system, immune regulation, lipid metabolism.Involved in lipid metabolism is the main function of ApoE, as a component of very low densitylipoprotein (VLDL) and chylomicron particles (CM), it can remove the residual of VLDL andCM in the blood and regulating serum lipid concentration; as low density lipoprotein (LDL)receptor ligands, it can mediated LDL tissue absorption; as a component of the high-densitylipoprotein (HDL) cholesterol, it participate the cholesterol efflux. Given the important role ofApoE in lipid metabolism, ApoE knockout models are widely used, the model appears lipidmetabolic disorder and hyperlipidemia in the normal diet, so it is used to study the pathogenesisof hyperlipidemia and ideal model of intervention measures. Domestic and foreign researchfocused on atherosclerosis and drug screening.Steroid hormone is sex hormones and utilize cholesterol as the substrate of synthetic, it hasvery important physiological functions, mainly includs estrogen, testosterone, progesterone, theyplay an important role in the regulation of reproduction. Due to steroid hormones has closecontact with cholesterol and reproductive, our lab use ApoE-/-model to study the effect of ApoEon the reproductive ability of mice, it is the first time in the world. Results shows that the ApoEknockout mice appear severe hyperglycemia, lipid metabolic disorder, lipid accumulation in theovary, cause ovarian overweight, estrus cycle in in ApoE-/-mice after sexual maturity is disorder,estrus days significantly lower than the wild type. ApoE-/-mouse at birth has much more folliclescompared to WT counterpart, while at D100the number of follicles has significant decreasedrelative to the wild type, suggests that the lack of ApoE brings certain effect to the folliculardevelopment of mice. The experiment on the basis of previous studies, continue to explore whatthe mechanism of ApoE loss cause the defect of follicle development. This study selected thefour days after birth (4D), and100days (D)100mouse ovaries, first of all, phosphatidyl inositol-3(PI3K) signaling pathway related genes serine threonine protein kinase1(Akt1), theBCL-2related to cell death activator (Bad), mammals rapamycin target protein (mTOR), nuclearfactor kappa b (Nfkb), phosphatase and tensin homolog (Pten), tuberous sclerosis complex2(Tsc2) and steroid hormone synthesis related genes cytochrome p450aromatase (Cyp19a1),3beta hydroxy steroid dehydrogenase (Hsd3b) expression quantity were studied. Real-time PCRresults show that at D100in ApoE-/-mice, Cyp19a1Hsd3b, mTOR, Nfkb, relative to the wild typemice dropped significantly, while Bad and Tsc2increase sharply. At D4, the Hsd3b and mTORin ApoE-/-mice expression significantly raised. Next we selected the wild type and ApoE-/-mice56days after born (D56), and100days after birth (D100),estrogen and progesterone levels inthe serum of mice were tested. All the mice in proestrus. Results shows that at D100, serumestrogen and progesterone levels in the ApoE-/-mice significantly lower than the wild type, andthere was no significant change in56D. We concluded that the disorder of follicles developmentmay results from the PI3K signaling pathway and steroid hormone synthesis related genes havean abnormal expression in the response of ApoE absent. |
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