A Study of Kir6.2 Gene Sequence in Rat Model of Type 2 Diabetes Mellitus Treated by CSN1S2 Protein of Etawah Crossbred Goat Milk

Abstract

Abstract Type 2 diabetes mellitus (T2DM) is a metabolic disease characterized by hyperglycemia. High blood glucose levels in T2DM patients are treated by sulfonylurea. However, the long-term use of sulfonylurea can affect the regulation of glucose homeostasis and cause hypoglycemia. The cascade gene associated with the hypoglycemia is Kir6.2, a constituent of ATP-sensitive potassium channel (KATP), in the neuron. Kir6.2 mutations cause dysregulation of insulin secretion by pancreatic beta cells and glucagon secretion by pancreatic alpha cells. The aim of this study was to analyze the effect of CSN1S2 protein of etawah crossbred goat milk on Kir6.2 gene sequences in the rat model of T2DM. The experimental animals used were male Wistar rats (Rattus norvegicus) which were divided into two major groups, namely control group and T2DM group. Each group was administrated by CSN1S2 protein with the dose of 375 mg/kg BW, 750 mg/kg BW, 1500 mg/kg BW, and without CSN1S2 protein administration. Each group was replicated three times. DNA was isolated from the rat brain. Kir6.2 gene was amplified by using specific primers. PCR products were purified and sequenced by using ABI 3730xl DNA Sequencer. DNA sequences were analyzed by using MEGA7 software. Amplification of the Kir6.2 gene produced 1173 bp DNA. There was no change in the Kir6.2 sequence in all treatments. The 25 mg/kg BW dose of streptozotocin had no effect on Kir6.2 gene sequence in the rat brain. This study also showed that administration of CSN1S2 protein at the dose of 375 mg/kg BB, 750 mg/kg BW, and 1500 mg/kg BW did not cause mutations in the Kir6.2 gene in the brain of the rat model of T2DM.