Fructose Sweetens the Deal

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Science  24 Feb 2012:
Vol. 335, Issue 6071, pp. 892-893
DOI: 10.1126/science.335.6071.892-d

Glucose, a metabolic product of dietary sucrose, triggers pancreatic beta cells to release insulin, which in turn allows many different cells types to take up glucose to store or use as energy. The other breakdown product of sucrose is fructose, and Kyriazis et al. report that it too plays a role in controlling insulin release. Fructose activates a sweet taste receptor (the TIR2-TIR3 heterodimer) expressed by mouse and human beta cells. This enhances the effect of glucose on insulin release. Mice injected with fructose (or saccharine, another taste receptor ligand) showed a rapid increase in circulating insulin, but only if functional taste receptors were present and only if glucose stimulated beta cells as well.

Fructose-activated sweet taste receptors signal through a phosphoinositide pathway, which elevates cytoplasmic Ca2+ concentration and depolarizes the membrane via a cation channel, TRPM5. Functional interaction between these two pathways is not yet clear, but because TRPM5 has been implicated in glucose-stimulated insulin secretion, it may be a convergence point. Whatever the mechanism, these findings may have implications for the link between high fructose consumption and the development of metabolic diseases such as obesity and diabetes.

Proc. Natl. Acad. Sci. U.S.A. 109, 10.1073/pnas.1200797109 (2012).

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