Abstract
Background Although glucose is indispensable for the stimulation of insulin release, numerous other insulin secretagogues have been identified. For instance, the dietary monosaccharide fructose potentiates insulin secretion in vitro, but the mechanism and physiological significance remains unclear. The T1R2-T1R3 heterodimer of G protein-coupled receptors mediates sweet sensing in the tongue and ablation of either subunit obliterates sweet taste. We hypothesized that the effects of fructose on insulin release may be mediated by sweet taste receptors (TRs) on beta-cells.
Highlights
Glucose is indispensable for the stimulation of insulin release, numerous other insulin secretagogues have been identified
Fructose (10.0mM) rapidly activated Phospholipase C (PLC) and increased intracellular calcium (Ca2+i) and insulin release at 8.3mM glucose in wild type (WT) islets and MIN6 cells, but these effects were absent in T1R2 knockout (T1R2-/-) islets
Glucose-stimulated insulin release (GSIS) in WT mice was potentiated by low physiological concentrations of fructose (3.0mM in vitro; 0.3g/kg in vivo), but these effects were absent in T1R2-/- mice
Summary
Glucose is indispensable for the stimulation of insulin release, numerous other insulin secretagogues have been identified. The dietary monosaccharide fructose potentiates insulin secretion in vitro, but the mechanism and physiological significance remains unclear. The T1R2-T1R3 heterodimer of G protein-coupled receptors mediates sweet sensing in the tongue and ablation of either subunit obliterates sweet taste. We hypothesized that the effects of fructose on insulin release may be mediated by sweet taste receptors (TRs) on beta-cells
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