[EFFECT OF T1R3 RECEPTOR PROTEIN DELETION ON GLUCONEOGENESIS AND LIPID METABOLISM IN MICE]

Receptors of the T1R family are molecular sensors for sweet taste stimuli. They are expressed not only in the oral cavity, but in most of endocrine cells controlling homeostasis of glucose as well as in adipocytes. Earlier, we have demonstrated that deletion of the Taslr3 gene, which encodes the T1R3 protein, reduces glucose tolerance, elevates insulin resistance and cause a decrease of blood glucose level after food deprivation. The goal of the study was to elucidate an involvement of T1R3 in control of endogenous glucose synthesis and lipid metabolism. Experiments were performed with an inbred mouse strain C57BL/6ByJ and the Taslr3-gene knockout strain C57BL/6J-Tas1r3tm1Rfm maintained at the normocaloric diet. It was shown in vivo that the presence of intact T1R3 stimulates gluconeogenesis and lipid utilization during starvation and likely promotes glycogen synthesis. Additionally, T1R3 potentiates utilization of triglycerides and glycerol (in fed state) and restricts secretion of glucagon during fasting but does not affect insulin output. Thus, T1R3-mediated visceral reception of metabolites is involved in control of carbohydrate and lipid metabolism.