Inhibitory Effect And Mechanism Of Catechins On The Differentiation Of Mouse 3T3-L1 Preadipocytes

As a metabolic disease,obesity is mainly caused by the accumulation of fat due to the proliferation and differentiation of preadipocytes in the body.Obesity is not only the change of body weight,but also induces the occurrence of various diseases such as cardiovascular disease and diabetes etc.Four main catechin monomers were selected in this experiment:Epicatechin(EC),Epicatechin gallate(ECG),Epigallocatechin(EGC)and Epigallocatechin gallate(EGCG)and their inhibitory effect of mouse 3T3-L1 adipocyte differentiation was studied,the inhibitory mechanism of adipocyte differentiation was further explored and clarified through transcriptomics and lipidomics.The main findings are as follows:1.Different concentrations(10 μM,30 μM,50 μM)of catechin monomers(EC,EGC,ECG,EGCG)were used to interfere with the differentiation processof mouse 3T3-L1 preadipocytes.According to the results of lipid staining,the contents of intracellular triglyceride,and total cholesterol evaluation,the catechin monomer EGCG with the strongest activity to inhibit the differentiation of 3T3-L1 preadipocytes was screened,and the optimal concentration of EGCG to inhibit the differentiation was 50 μM.2.Transcriptome analysis showed that there were 4,299 significantly different genes between the EGCG experimental and control groups.GO analysis showed that the number of genes enriched in regulating adipocyte differentiation was the largest,among which Ptgs2 and Pim1 had the largest fold difference;KEGG analysis found that genes related to lipid metabolism were mainly enriched in MAPK and Fox O signaling pathways.3.Lipidomics analysis revealed 146 significantly different metabolites between the EGCG experimental group and the control group,KEGG enrichment analysis of differential lipids,combined with transcriptome data,found that EGCG up-regulated Pla2g2 e gene and down-regulated Pla2g4 a and Pla2g2 a genes through the glycerophospholipid metabolic pathway to up-regulate Lyso-phosphatidylcholine(LPC)expression,thereby affecting the differentiation process of 3T3-L1 preadipocytes.