Insulin release: the receptor hypothesis

Abstract

It is currently believed that the stimulation of insulin release by nutrient secretagogues reflects their capacity to act as fuel in pancreatic islet beta cells. In this review, it is proposed that such a fuel concept is not incompatible with a receptor hypothesis postulating the participation of cell-surface receptors in the recognition of selected nutrients as insulinotropic agents. Pursuant to this, attention is drawn to such matters as the anomeric specificity of the beta cell secretory response to D-glucose and its perturbation in diabetes mellitus, the insulinotropic action of artificial sweeteners, the possible role of bitter taste receptors in the stimulation of insulin secretion by L-glucose pentaacetate, the recently documented presence of cell-surface sweet taste receptors in insulin-producing cells, the multimodal signalling process resulting from the activation of these latter receptors, and the presence in beta cells of a sweet taste receptor mediating the fructose-induced potentiation of glucose-stimulated insulin secretion.

Lactisole inhibits the glucose-sensing receptor T1R3 expressed in mouse pancreatic β-cells

“…We have shown recently that T1R3, a subunit of the sweet taste receptor (Nelson et al 2001, Temussi 2007, functions as a glucose-sensing receptor in b-cells (Malaisse 2014, Kojima et al 2015. This receptor is activated by glucose, and promotes metabolism of fuels in b-cells leading to an increase in ATP .…”

Associations Among Taste Perception, Food Neophobia and Preferences in Type 1 Diabetes Children and Adolescents: A Cross-Sectional Study

“…Contradictory results were also reported when the associations between taste impairment and metabolic control, disease duration, and the presence of diabetes-related complications were studied [10,11,15]. However, this field of research remains largely unexplored.…”

“…Variation in taste responsiveness to PROP has been linked to various health disorders, including obesity [13] and diabetes [14]. However, related data are still scarce and controversial, probably due to differences in the methodologies used to evaluate taste perception and the involved subjects (e.g., those affected by type 1 or type 2 diabetes).Contradictory results were also reported when the associations between taste impairment and metabolic control, disease duration, and the presence of diabetes-related complications were studied [10,11,15]. However, this field of research remains largely unexplored.Notably, to the best of our knowledge, studies evaluating taste perception in children and adolescents affected by T1D are lacking globally.…”

Steviol glycosides enhance pancreatic beta-cell function and taste sensation by potentiation of TRPM5 channel activity

“…Specific TRPM5 polymorphisms showed increased prevalence in patients with obesity-related metabolic syndrome18. On the basis of these observations, the hypothesis was developed that TRPM5 might be a pharmacological target for the development of a novel type of insulin secretagogue192021. However, since pharmacology for TRPM5 is currently limited to fairly non-selective-blocking agents, this hypothesis remained untested22232425.…”