Sensory Systems for Sugar-Induced Cephalic Phase Insulin Release

Abstract

Abstract Purpose of Review This review aims to discuss and summarize the peripheral sensory mechanisms involved in the induction of the early phase of insulin release, known as cephalic phase insulin release (CPIR), triggered by stimuli related to food, particularly sugars. Recent Findings At least, two distinct systems on the tongue are responsible for detecting oral sugars. The first system involves the G-protein-coupled receptor Tas1r2/Tas1r3, which can detect not only sugars but also artificial sweeteners and sweet proteins. The second system relies on glucose transporters, specifically recognize and transport monosaccharides. The Tas1r2/Tas1r3 receptor utilizes a signal transduction pathway involving gustducin, phospholipase β2, and transient receptor potential channel M5 to depolarize taste cells. On the other hand, glucose transporters facilitate the transport of monosaccharides into cells, where their degradation produces ATP. This ATP inhibits the metabolic sensor KATP channel, ultimately leading to cell depolarization. Recent studies in mice have demonstrated that glucose transporters and KATP channels, rather than the Tas1r2/Tas1r3 receptor, are essential for the induction of CPIR. Summary The detection of sugars in the oral cavity relies on two essential mechanisms: the Tas1r2/Tas1r3 receptor and glucose transporters. Notably, oral glucose transporters are likely to play a significant role in the induction of sugar-induced CPIR. As a result, these two sugar detection systems may have distinct roles in maintaining energy homeostasis within the body.