Metal Ion Transportation Patterns and Chemokines Level Highlight from the Point of View of the Innate Immune System in the Formation of Non-alcoholic Fatty Liver Disease

Abstract

Purpose: Non-alcoholic fatty liver disease (NAFLD), including non-alcoholic fatty liver (NAFL) and non-alcoholic steatohepatitis (NASH), represents the hepatic manifestation of obesity and metabolic syndrome. NAFLD covers a spectrum of disorders ranging from simple steatosis to non-alcoholic NASH and cirrhosis, which properly can develop into liver cancer. In our research, we use bioinformatics methods to evaluate the biological progress changes from normal liver to non-alcoholic fatty liver disease. Method: We downloaded the data from the NCBI GEO database and begin the analysis of the GSE151158, after using three common different expression genes analysis of R language, including edgR, DESeq2, and limma. We found the common gene set in the transcriptional progress which contains 270 genes in the threshold of p<0.05. After that, Gene set enrichment analysis(GSEA) is performed to find the important biological function or module in the formation of Non-alcoholic fatty liver disease. Results: By using the bioinformatics method, we found 270 differently expressed genes(DEGs) in the progress of formation of Non-alcoholic fatty liver disease. Gene set enrichment analysis is performed to find the enriched functions. We found that 13 metal ion transport or metabolism-related and 3 chemokine-related genes were enriched. The metal ion transport or metabolism-related genes mostly get negative enrichment scores, while most chemokines-related genes got positive enrichment scores. Conclusion: The results we obtained from the research meant that metal ion transportation patterns and abnormal chemokines played several key roles from the point of view of the innate immune system in the formation of non-alcoholic fatty liver disease. As an early stage of non-alcoholic fatty liver disease, this finding will help us to understand the disease mechanism and design effective drugs to prevent the development and deterioration of the non-alcoholic fatty liver disease.