eISSN: 2221-6197 DOI: 10.31301/2221-6197

Association of two single nucleotide variants of the GIPR gene with type 2 diabetes mellitus

Year: 2026

Pages: 105-114

Number: Volume 18, issue 1

Type: scientific article

Summary:

Type 2 diabetes mellitus (T2DM) is a chronic disease in which the body is unable to effectively utilize the insulin produced by the pancreatic cells.  The GIPR gene plays a key role in regulating eating behavior in people with T2DM, influencing appetite and satiety control through the central nervous system. The GIPR gene is a key link between nutrition, the brain, and metabolism. Genetic polymorphisms in this gene may predispose people to eating disorders, which, combined with a direct effect on insulin secretion, significantly increases the overall risk of developing T2DM. The purpose of this study was to analyze the associations between polymorphic markers rs2302382 and rs1800437 in the GIPR gene and the development of T2DM, the presence of eating disorders, and metabolic biochemical parameters in the Tatar ethnic group living in the Republic of Bashkortostan. The study was conducted in 197 patients with T2DM and 379 control subjects. An association was determined between the polymorphic variant GIPR rs2302382 and the risk of developing T2DM in recessive (OR=2.07, P=0.01) and additive models (OR=1.29, P=0.023). An association with the development of T2DM was found for GIPR rs1800437 polymorphism in the recessive model (OR=2.85, P=0.0093). An association was identified between the CC genotype of the rs1800437 GIPR gene marker and cholesterol levels (P=0.018). The rs2302382 marker was associated with increased glycated hemoglobin HbA1c P=0.046. Thus, a genetically determined change in the function of the GIPR gene may be the starting point that, through its influence on the brain and behavior and directly on metabolic changes, triggers a cascade leading to the development of type 2 diabetes.

Keywords:

type 2 diabetes mellitus, obesity, eating behavior, gastric inhibitory polypeptide receptor, β-cells, insulin.

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eISSN: 2221-6197 DOI: 10.31301/2221-6197