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STIM1 regulates calcium signaling in taste bud cells and preference for fat in mice
Gado Dramane, … , Philippe Besnard, Naim Akhtar Khan
Gado Dramane, … , Philippe Besnard, Naim Akhtar Khan
Published May 1, 2012
Citation Information: J Clin Invest. 2012;122(6):2267-2282. https://doi.org/10.1172/JCI59953.
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Research Article Metabolism

STIM1 regulates calcium signaling in taste bud cells and preference for fat in mice

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Abstract

Understanding the mechanisms underlying oro-gustatory detection of dietary fat is critical for the prevention and treatment of obesity. The lipid-binding glycoprotein CD36, which is expressed by circumvallate papillae (CVP) of the mouse tongue, has been implicated in oro-gustatory perception of dietary lipids. Here, we demonstrate that stromal interaction molecule 1 (STIM1), a sensor of Ca2+ depletion in the endoplasmic reticulum, mediates fatty acid–induced Ca2+ signaling in the mouse tongue and fat preference. We showed that linoleic acid (LA) induced the production of arachidonic acid (AA) and lysophosphatidylcholine (Lyso-PC) by activating multiple phospholipase A2 isoforms via CD36. This activation triggered Ca2+ influx in CD36-positive taste bud cells (TBCs) purified from mouse CVP. LA also induced the production of Ca2+ influx factor (CIF). STIM1 was found to regulate LA-induced CIF production and the opening of multiple store-operated Ca2+ (SOC) channels. Furthermore, CD36-positive TBCs from Stim1–/– mice failed to release serotonin, and Stim1–/– mice lost the spontaneous preference for fat that was observed in wild-type animals. Our results suggest that fatty acid–induced Ca2+ signaling, regulated by STIM1 via CD36, might be implicated in oro-gustatory perception of dietary lipids and the spontaneous preference for fat.

Authors

Gado Dramane, Souleymane Abdoul-Azize, Aziz Hichami, Timo Vögtle, Simon Akpona, Christophe Chouabe, Hassimi Sadou, Bernhard Nieswandt, Philippe Besnard, Naim Akhtar Khan

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