| Abstract of study | Type 2 diabetes mellitus (T2DM) is a complex disease that is caused by an impairment in the secretion of β-cell insulin and by a peripheral resistance to insulin. Most patients suffering from T2DM and from obesity exhibit insulin resistance in the muscles, liver, and fat, resulting in a reduced response of these tissues to insulin. In healthy individuals, pancreatic islet β-cells secrete insulin to regulate the increase in blood glucose levels. Once these β-cells fail to function, T2DM develops. Despite the progress achieved in this field in recent years, the genetic causes for insulin resistance and for T2DM have not yet been fully discovered. The present study aims to characterize T2DM by comparing its gene expression with that of normal controls, as well as to identify biomarkers for early T2DM. Gene expression profiles were downloaded from the Gene Expression Omnibus, and differentially expressed genes (DEGs) were identified for type 2 diabetes. Furthermore, functional analyses were conducted for the gene ontology and for the pathway enrichment. In total, 781 DEGs were identified in the T2DM samples relative to healthy controls. These genes were found to be involved in several biological processes, including cell communication, cell proliferation, cell shape, and apoptosis. We constructed a protein-protein interaction (PPI) network, and the clusters in the PPI were analyzed by using ClusterONE. Six functional genes that may play important roles in the initiation of T2DM were identified within the network. |