[Exposure of beta-cells to chronic fructose potentiates glucose-stimulated insulin secretion through ATP signaling].

While the use of fructose as a sweetener and its consumption are associated with increased fat storage prompted by the action of insulin, fructose alone does not acutely stimulate insulin exocytosis from the pancreatic beta-cell, as opposed to the chief secretagogue glucose. We investigated the effects of chronic exposure to fructose on beta-cell function. Our results reveal that chronic fructose induces extracellular ATP signaling in the beta-cell, resulting in the potentiation of glucose-stimulated insulin secretion. This effect is mediated by the activation of the purinergic P2Y1 receptors and is associated with the release of cellular ATP through pannexin-1 channels. Consequently, the interplay between pannexin channels and purinergic receptors, through ATP signaling, represents a novel cellular target with potential therapeutic implications.