Effects Of Maternal Obesity And High Fat Diet During Pregnancy On Placental Nutrienttransport And Fetal Growth In Utero In Rats

Objective In the study,rat obesity model was induced by high fat diet. We observed intrauterine fetal growth and placental development in obese pregnancy rats, and examined the expression of placental nutrients transporters. The aim of this study was to explore the mechanism of offspring abnormal intrauterine growth and development caused by maternal obesity. Methods Seven weeks old female Spague-Dawlay(SD) rats were fed with high fat diet for 8 weeks. Diet induced obesity(DIO) rats and diet induced obesity resistant(DIR) rats were picked up from HFD group according body weight gain. DIO and DIR rats were fed with high fat diet during pregnancy. The rats in control group were divided into two groups, rats in one group were fed with normal diet, and the otherwas given high-fat diet. Food intake during pregnancy was recorded. At GD21, pregnant rats were sacrificed after anesthesia. Fetal body weight and crown-rump length, placental weight and diameter were measured. RT-PCR was used to detect mRNA expression levels of placental glucose transporter(glut1), amino acid transporter(snat2) and fatty acid transporter(cd36, fatp1, fatp4). Placental amino acid transporter(CD36, FATP1, FATP4) protein expression levels were detected by Western Blot. Results After high fat diet for 8 weeks, body weight of DIO rats was significantly higher than rats in control group(21.2%, P <0.05). There was no significant difference in body weight between DIR rats and CON rats. There was significant difference in food intake and energy intake among three groups(F = 7.477, P = 0.002; F = 28.412, P < 0.001). Compared with the CON group, serum TC level of DIR rats before pregnancy increased significantly(P <0.05); serum TG level of rats was significantly elevated in DIO group(P <0.05). At GD0, body weight of DIO-H rats was significantly higher than body weight of rats in the other three groups(P <0.05). There was significant difference in food intake and energy intake during pregnancy among four groups(F = 3547, P = 0.028; F = 9.848, P < 0.001). At GD21, there was no significant difference in FBG and serum insulin level among four groups(F = 2.163, P = 0.109; F = 0.709, P = 0.506). There was significant difference in fetal weight among four groups(F = 3.004, P = 0.043). Compared with the C-C group, fetal weight in DIO-H group significant decreased(P <0.05). There was significant difference in fetal weight to placental ratio among four groups(F = 7.675, P < 0.001). The ratio in DIO-H group was higher than that in C-C group(P <0.05). There was no significant difference in placental glut1 and snat2 level among four groups. Placental cd36, fatp1 and fatp4 were obviously down-regulated in DIO-H rats(P <0.05). Compared with C-C rats, placental CD36, FATP1 and FATP4 protein expression were obviously lower in DIO-H rats(P <0.05). Conclusion The results of the study showed that maternal obesity led to intrauterine growth retardation, and down-regulated the expression of placental fatty acid transporter(CD36, FATP1, FATP4). It prompted that maternal obesity led to intrauterine growth retardation, by down-regulating the expression of placental fatty acid transporter, and then disturbed placental fatty acid transport. The results may provide scientific experimental basis for the prevention of intrauterine dysplasia caused by maternal obesity.