Abstract
Aims: To identify the key differentially expressed genes (DEGs) in islet and investigate their potential pathway in the molecular process of type 2 diabetes.Methods: Gene Expression Omnibus (GEO) datasets (GSE20966, GSE25724, GSE38642) of type 2 diabetes patients and normal controls were downloaded from GEO database. DEGs were further assessed by enrichment analysis based on the Database for Annotation, Visualization and Integrated Discovery (DAVID) 6.8. Then, by using Search Tool for the Retrieval Interacting Genes (STRING) 10.0 and gene set enrichment analysis (GSEA), we identified hub gene and associated pathway. At last, we performed quantitative real-time PCR (qPCR) to validate the expression of hub gene.Results: Forty-five DEGs were co-expressed in the three datasets, most of which were down-regulated. DEGs are mostly involved in cell pathway, response to hormone and binding. In protein–protein interaction (PPI) network, we identified ATP-citrate lyase (ACLY) as hub gene. GSEA analysis suggests low expression of ACLY is enriched in glycine serine and threonine metabolism, drug metabolism cytochrome P450 (CYP) and NOD-like receptor (NLR) signaling pathway. qPCR showed the same expression trend of hub gene ACLY as in our bioinformatics analysis.Conclusion: Bioinformatics analysis revealed that ACLY and the pathways involved are possible target in the molecular mechanism of type 2 diabetes.
Highlights
According to International Diabetes Federation (IDF) reports, there were 425 million diabetic patients worldwide in 2017, of which type 2 diabetes accounted for more than 90%
A total of 2536 Differentially expressed gene (DEG) were obtained in GSE20966
Shao et al [13] identified that the glucocorticoid was central in the pathogenesis of type 2 diabetes from three Gene Expression Omnibus (GEO) datasets by integrated method including DEGs screen, gene functional enrichment, protein–protein interaction (PPI) network analyses, drug–gene interactions and genetic association of DEGs
Summary
According to International Diabetes Federation (IDF) reports, there were 425 million diabetic patients worldwide in 2017, of which type 2 diabetes accounted for more than 90%. It is estimated that in 2045 the number of people with diabetes will increase to 629 million [1]. Diabetes often leads to cardiovascular complications, which have a serious impact on the patient’s life and quality of life, and cause a heavy social burden. The pathophysiological mechanism of type 2 diabetes is still not very clear at present. It is currently believed that type 2 diabetes is mainly caused by genetic factors and the environmental influence [2,3]. The genetic cause accounts for a part of the etiology in type 2 diabetes. To prevent and reduce the complications of type 2 diabetes, it is especially important to clarify the pathophysiological mechanism at genetic level
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