Analysis of Genetic Polymorphisms of OCT1, MATE1, MATE2 and GLP1R in Rats with Experimentally Induced Obesity

Abstract The experimental model of obesity based on a cafeteria diet is a common model to investigate different aspects of obesity. The present study aimed to evaluate the link between genetic variants of OCT1, MATE1, MATE2 and GLP1R and the treatment effects in male obese rats. After 19-weeks of feeding with a standard chow food and Cafeteria-diet (CAF), the rats were divided into three groups: control group (only CAF), metformin group (CAF and metformin treatment) and liraglutide group (CAF and GLP1 agonist treatment). The genetic variations of the receptors for metformin in liver and kidney (OCT1, MATE1, MATE2) and for liraglutide (GLP1R) were examined. The results demonstrated a significant decrease in body mass index, blood glucose and a significant increase in plasma HDL-cholesterol levels in both groups treated with either metformin or liraglutide compared to the control group. No effect on plasma triglycerides and VLDL-cholesterol levels was shown between the three groups. According to the genetic analysis, all rats were “wild type” for the genetic variants tested in OCT, MATE1, MATE2 and GLP1R, not affecting the effects of treatment. This raises the possibility of other potential genes implicated in the underlying mechanism of obesity and metformin/liraglutide therapy.