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Cited by 232

The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.

Sweet taste receptor signaling in beta cells mediates fructose-induced potentiation of glucose-stimulated insulin secretion

Open access
Kyriazis, George A., Soundarapandian, Mangala M., Tyrberg, Björn·2012·Proceedings of the National Academy of Sciences

Abstract

Postprandial insulin release is regulated by glucose, but other circulating nutrients may target beta cells and potentiate glucose-stimulated insulin secretion via distinct signaling pathways. We demonstrate that fructose activates sweet taste receptors (TRs) on beta cells and synergizes with glucose to amplify insulin release in human and mouse islets. Genetic ablation of the sweet TR protein T1R2 obliterates fructose-induced insulin release and its potentiating effects on glucose-stimulated insulin secretion in vitro and in vivo. TR signaling in beta cells is triggered, at least in part, in parallel with the glucose metabolic pathway and leads to increases in intracellular calcium that are dependent on the activation of phospholipase C (PLC) and transient receptor potential cation channel, subfamily M, member 5 (TRPM5). Our results unveil a pathway for the regulation of insulin release by postprandial nutrients that involves beta cell sweet TR signaling.

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Metadata

Authors
Kyriazis, G. A., Soundarapandian, M. M., & Tyrberg, B.
Venue
Proceedings of the National Academy of Sciences
Published
2012-02-06
Volume
109
Issue
8
Pages
E524-32
ISSN
  • 0027-8424 (ISSN-L)
  • 1091-6490
OpenAlex
W2163903769
Cited by
232
References
3
FWCI
22.55
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: Sweet taste receptor signaling in beta cells mediates fructose-induced potentiation of glucose-stimulated insulin secretion. https://app.cochat.ai/papers/10.1073/pnas.1115183109
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Kyriazis, G. A., Soundarapandian, M. M., & Tyrberg, B. (2012). Sweet taste receptor signaling in beta cells mediates fructose-induced potentiation of glucose-stimulated insulin secretion. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.1115183109

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