T1R3 protein, the main subunit of the sweet taste receptor and receptor of amino acid taste, is expressed in the epithelium of the tongue and gastrointestinal tract, in β cells of the pancreas, hypothalamus, and numerous other organs. Recently, convincing evidences on the involvement of T1R3 in the control of carbohydrate and lipid metabolism, and the control of incretin and insulin production were obtained. In the study on Tas1r3-gene knockout mouse strain and parent C57BL/6J strain as a control, the data on the effect of T1R3 on morphological characteristics of Langerhans islets in the pancreas were obtained. In Tas1r3 knockout animals, we found a reduction in the size of islets and their density in pancreatic tissue as compared to the parent strain. In addition, a decrease in the expression of active caspase-3 in the islets of gene-knockout mice was demonstrated. The data obtained indicate that the lack of functioning gene encoding sweet taste receptor protein causes a dystrophy of the islet tissue and is associated with the development of pathological changes in the pancreas specific to type 2 diabetes mellitus and obesity in humans.
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