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Sweet taste receptors in rat small intestine stimulate glucose absorption through apical GLUT2

Mace, O.J., Affleck, J., Patel, N. and Kellett, G.L. (2007) Sweet taste receptors in rat small intestine stimulate glucose absorption through apical GLUT2. Journal of Physiology, 582 (1). pp. 379-392. ISSN 0022-3751

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Natural sugars and artificial sweeteners are sensed by receptors in taste buds. T2R bitter and T1R sweet taste receptors are coupled through G-proteins, α-gustducin and transducin, to activate phospholipase Cβ2 and increase intracellular calcium concentration. Intestinal brush cells or solitary chemosensory cells (SCCs) have a structure similar to lingual taste cells and strongly express α-gustducin. It has therefore been suggested over the last decade that brush cells may participate in sugar sensing by a mechanism analogous to that in taste buds. We provide here functional evidence for an intestinal sensing system based on lingual taste receptors. Western blotting and immunocytochemistry revealed that all T1R members are expressed in rat jejunum at strategic locations including Paneth cells, SCCs or the apical membrane of enterocytes; T1Rs are colocalized with each other and with α-gustducin, transducin or phospholipase Cβ2 to different extents. Intestinal glucose absorption consists of two components: one is classical active Na+–glucose cotransport, the other is the diffusive apical GLUT2 pathway. Artificial sweeteners increase glucose absorption in the order acesulfame potassium sucralose > saccharin, in parallel with their ability to increase intracellular calcium concentration. Stimulation occurs within minutes by an increase in apical GLUT2, which correlates with reciprocal regulation of T1R2, T1R3 and α-gustducin versus T1R1, transducin and phospholipase Cβ2. Our observation that artificial sweeteners are nutritionally active, because they can signal to a functional taste reception system to increase sugar absorption during a meal, has wide implications for nutrient sensing and nutrition in the treatment of obesity and diabetes.

Item Type: Article
Copyright, Publisher and Additional Information: Open access copy available from the journal web site.
Institution: The University of York
Academic Units: The University of York > Biology (York)
Depositing User: Open Access From Journal
Date Deposited: 23 Dec 2008 14:04
Last Modified: 23 Dec 2008 14:04
Published Version: http://dx.doi.org/10.1113/jphysiol.2007.130906
Status: Published
Publisher: Wiley-Blackwell
Refereed: Yes
Identification Number: 10.1113/jphysiol.2007.130906
URI: http://eprints.whiterose.ac.uk/id/eprint/5047

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