STIM1 regulates calcium signaling in taste bud cells and preference for fat in mice
Gado Dramane, Souleymane Abdoul-Azize, Aziz Hichami, Timo Vögtle, Simon Akpona, Christophe Chouabe, Hassimi Sadou, Bernhard Nieswandt, Philippe Besnard, Naim Akhtar Khan
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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Research Article Metabolism

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

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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Figure 3

Implication of AA and PLA2 in Ca2+ influx in CD36-positive TBCs.

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Implication of AA and PLA2 in Ca2+ influx in CD36-positive TBCs. (A) T...
(A) The CD36-positive TBCs (2 × 106/assay) were loaded with Fura-2/AM, as described in Methods. The experiments were performed in Ca2+-free medium. The arrows indicate when the test molecules, TG (5 μM), AA (0, 10, 20 μM), and CaCl2 (1.5 mM), were added. The histograms show mean ± SEM of 7 independent experiments. *P < 0.001 compared with control (CaCl2). Indo and 1-ABT were used at 10 μM with AA. (B) Effect of different PLA2 inhibitors on Ca2+ influx. The experiments were performed in Ca2+-free medium. The arrows indicate when the test molecules, i.e., PLA2 inhibitors (15 μM), TG (5 μM), or CaCl2 (1.5 mM), were added. “No inhibitor” trace shows the recording in the absence of PLA2 inhibitors. The histograms show the results, obtained from the traces, as mean ± SEM (n = 7). *P < 0.001 compared with control, CaCl2. All of these experiments were performed in a PTI spectrofluorometer. (C) Ca2+ influx after transfection of CD36-positive TBCs by siRNA of different sPLA2 isoforms. Experiments were performed as in B.