Abstract :
Death and dysfunctionality of pancreatic islet beta-cells are a centric key element in the pathogenesis of type 2 diabetes mellitus (T2DM). Saturated fatty acids are commonly circulated in diabetic and obese individuals. Elevated and chronic exposure to fatty acids has a pernicious influence on islet cells’ functionality and survival due to its capability to induce apoptosis and endoplasmic reticulum (ER) stress. However, T2DM is a heterogeneous disorder that includes genetic and environmental factors in conjunction with dyslipidaemia with a considerably high rate of morbidity and mortality. There are many genes involved in the pathogenesis that remain to be charted. Here, we show a comprehensive interrogation of GATA6 based on previously published gene expression data on the basis of stating its validity via bioinformatics analysis and reaching a new understanding. Various datasets with different patient cohorts were compared and contrasted. Gene ontology and predictive pathway analysis (e.g., Kyoto Encyclopaedia of Genes and Genomes pathway; KEGG) were used to explore interactions of numerous differentially expressed genes. Protein-protein interactions network through the STRING database has appreciated a list of key genes. GATA6 interacted with genes from pathways that were significantly enriched (FDR
Keyword :
GATA6, Pancreatic beta cells, T2DM, ER stress, Expression data, Bioinformatics analysis.