| Maternal high fat diet during pregnancy can lead to imbalance of intrauterine nutrition,when the offspring cope with this stressful environment,the body’s metabolic related genes,such as genes related to inflammation and glycolipid metabolism,are widely activated,resulting in metabolic abnormalities in the offspring.Our previous study also showed that maternal high fat diet during pregnancy can cause obesity,diabetes,NAFLD and other metabolic diseases in adulthood.However,the specific mechanism of metabolic abnormalities in offspring caused by it is still unclear.In this study,we will discuss this.Methods: All female 3-week Sprague-Dawley rats were randomly divided into two groups,fed a normal diet(CON group)and a high fat diet(HFD group)for 8weeks,at 11 weeks of age,they were mated with normal male rats.After full-term pregnancy,the expression of inflammatory factors in the placenta of prenatal female rats,the expression of inflammatory factors in the umbilical cord blood and the expression of liver inflammatory factors and lipid metabolism related genes in neonatal rats were detected.The SCD1 gene was overexpressed in HepG2 cells and neonatal rats,and the lipid metabolism in cells and liver tissues was detected to determine the interaction between inflammation and SCD1 gene in lipid metabolism.The results showed that compared with the normal diet group,the levels of inflammatory factors IL6,TNF-α,IL-1β and CCR2 in the placenta of the high fat diet group were significantly increased;the expression levels of inflammatory factors IL6,IL-1β and CCR2 in umbilical cord blood and liver tissue were increased,while the expression of TNF-α was not significantly changed in both;compared with the F1 generation of the normal diet group,the fatty acid synthesis related genes(SREBP1c,FASN and SCD1)and the expression of the related genes(PPARα,CPT1α and ACSL3)in the liver of the F1 generation of the high fat diet group were all up-regulated,and the content of triglyceride in the liver was also increased(12.49±2.95umol/L and28.46±3.23umol/L);however,the cholesterol content did not change significantly.The level of HepG2 cell intracellular triglycerides changes with the expression level of SCD1;similarly,after overexpressing the SCD1 gene in neonatal rats,triglyceride content in the liver tissue increased(1324.20 ± 109.75 umol / L and 1691.78 ±70.68 umol / L),but the body weight,biochemical indicators and liver total cholesterol levels did not change.The above results indicate that maternal high fat diet can lead to an intrauterine inflammatory environment.When the offspring cope with this environment,the expression of lipid metabolism related-genes in the offspring liver changes,which leads to an increase in the triglyceride content in the liver tissue of the offspring,among which SCD1 may play an important role. |