Genetic investigation of TRAIL mechanism in diabetic obese and non-diabetic obese patients

Obesity is an important healthcare issue caused by abnormally increased adipose tissue because of energy-intake overcoming energy expenditure with a globally high prevalence. Disturbances in the physiological function of adipose tissue mediate the development of diabetes, which is divided into two main classes as Type-I(insulin-dependent) and Type-II(non-insulin-dependent) characterized by high-blood-glucose levels. It is a metabolic disease that results from decreased insulin-levels and/or changes in the insulin action mechanism. However, decreased response to insulin in adipose tissue causes the development of insulin-resistance. Tumor Necrosis Factor-Associated Apoptosis-Inducing Ligand(TRAIL), which is a member of the Tumor Necrosis Factor(TNF)-family with an important role in adipose tissue biology, is included in many studies with its ability to induce apoptosis in cancer cells, but the number of human-studies conducted on the gene related to its protective-role against diabetes and obesity at this level is insufficient. The RNA-isolation, cDNA-synthesis, Real-Time-PZR(RT-qPZR), and Sanger-Sequencing Methods were used in this study. It is the first study in which human TRAIL gene expression and sequencing were performed together. As a result of the analyses, TRAIL gene expression level was found to be higher in the controls than in the diabetic-obese and non-diabetic-obese group. This change in TRAIL gene expression suggests that TRAIL maybe a protective factor against diabetes. The presence of rs781673405, rs143353036, rs1244378045, rs201137623, rs767450259, rs759369504, rs750556128, and rs369143448 mutations, which was determined with the Sequencing Method, was shown for the first time in the present study. We believe that these data will make an important contribution to the literature.