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Insulin release: the receptor hypothesis
1Department of Biochemistry, Université Libre de Bruxelles, 808 Route de Lennik, 1070, Brussels, Belgium, malaisse@ulb.ac.be.
Diabetologia
|April 5, 2014
Summary
Nutrient secretagogues stimulate insulin release by acting as fuel and through cell-surface receptors. This review explores how nutrient recognition by receptors influences insulin secretion in pancreatic beta cells.
Area of Science:
- Endocrinology
- Cell Biology
- Metabolism
Background:
- Nutrient secretagogues are believed to stimulate insulin release by acting as fuel in pancreatic islet beta cells.
- This review proposes that a fuel concept is compatible with a receptor hypothesis for nutrient recognition.
Purpose of the Study:
- To review the role of cell-surface receptors in nutrient-stimulated insulin release.
- To explore the interplay between nutrient metabolism and receptor-mediated signaling in pancreatic beta cells.
Main Methods:
- Review of existing literature on nutrient sensing and insulin secretion.
- Analysis of studies investigating nutrient-specific signaling pathways in beta cells.
- Examination of the role of taste receptors in insulinotropic responses.
Main Results:
- D-glucose anomeric specificity and its alteration in diabetes mellitus are discussed.
- Insulinotropic effects of artificial sweeteners and L-glucose pentaacetate are examined.
- Presence and function of sweet taste receptors in insulin-producing cells are highlighted, including their role in fructose potentiation of glucose-stimulated insulin secretion.
Conclusions:
- Cell-surface receptors play a crucial role in recognizing nutrients as insulinotropic agents.
- Nutrient sensing involves multimodal signaling pathways activated by these receptors.
- Understanding these mechanisms offers insights into glucose homeostasis and diabetes mellitus.
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