GSE178322
Translatomics probes into the role of lycopene on improving hepatic steatosis induced by high-fat diet
Liver is an important organ for fat metabolism. Excessive intake of a high-fat/energy diet is a major cause of hepatic steatosis and its complications such as nonalcoholic fatty liver disease and nonalcoholic steatohepatitis. Supplementation with lycopene, a natural compound, is effective in lowering triglyceride levels in the liver, although the underlying mechanism at the translational level is unclear. In this study, mice were fed a high-fat diet (HFD) to induce hepatic steatosis and treated with or without lycopene. Translation omics and transcriptome sequencing were performed on the liver to explore the regulatory mechanism of lycopene in liver steatosis induced by HFD, and identify differentially expressed genes (DEGs). Overall design: Total RNA and ribosome-bound RNA were extracted from the livers of high-fat diet- (HFD) and High-fat diet plus lycopene (LYC)-fed mice, and the polyA+ mRNA was sequenced using Illumina HiSeq X Ten sequencer. The reads were mapped to RefSeq RNA reference sequences and the expression level were quantified by rpkM calculation.