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Abstract
Insulin secretion from pancreatic β cells is controlled by nutrients, hormones, and neurotransmitters. Unlike the latter, which work through classic receptors, glucose and most other nutrients do not interact with membrane receptors but must be metabolized by β cells to induce insulin secretion. Studies have revealed the presence of umami and sweet taste receptors and their downstream effectors in β cells. That the receptors are functional was established by the effects of fructose and artificial sweeteners, which induced signals similar to those produced in taste buds of the tongue. These signals mediated an increase in insulin secretion in the presence of glucose. However, the physiological implications of these pathways in insulin secretion are unclear because of the large differences between plasma concentrations of fructose or sweeteners and their effective concentrations in vitro.
