Taste Receptors Function as Nutrient Sensors in Pancreatic Islets: A Potential Therapeutic Target for Diabetes

Abstract

Glucose, amino acids, and free fatty acids are critical nutrients participating in stimulating or regulating the hormone secretion of islets. These nutrients are believed to be metabolized by pancreatic endocrine cells to function. However, recent evidence suggests that taste receptors, which play key roles in the oral cavity to sense glucose (sweet taste), amino acids (umami taste), and free fatty acids (fatty taste), are expressed in pancreatic islet cells and may act to sense these nutrients to regulate pancreatic hormone secretion, including insulin and glucagon. Disorders in these taste receptor pathways in islets may contribute to the pathogenesis of diabetes, or it may influence hyperglycemia, disturbance in amino acid metabolism, or hyperlipidemia. In this review, we su mMarize the expression and hormone-regulating functions of sweet, umami, and fatty taste receptors acting as nutrient sensors in pancreatic islets in vitro and in vivo. We discuss the potential roles of these taste receptor-nutrient sensor pathways in islets targeted to develop therapeutic strategies for diabetes and related disease.

Keywords: G protein-coupled receptors; Pancreatic islets; T1R2/T1R3; amino acids; diabetes; β cell glucose receptors.