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 10

Schematic representation of LA-induced Ca2+ signaling in CD36-positive TBCs.

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Schematic representation of LA-induced Ca2+ signaling in CD36-positive T...
LA binds to CD36 and leads to IP3 production (8) and depletes intracellular Ca2+ stores. Upon Ca2+ depletion, STIM1 will lose Ca2+ from its EF hand and be localized into punctate structures of the ER membranes, which are in close proximity to the plasma membrane. STIM1 triggers production of CIF that displaces inhibitory CaM from a plasma membrane–bound Ca2+-independent phospholipase A2 (iPLA2β), which produces Lyso-PC and free AA. The Lyso-PC will activate Orai1-dependent SOC channels that are responsible for SOCE. A massive Ca2+ influx via these channels may activate sPLA2 and cPLA2 and give rise to massive production of Lyso-PC and AA that will open Orai1 and Orai1/3 channels, respectively, and a massive increase in [Ca2+]i might be involved in exocytosis of neurotransmitters such as 5-HT, responsible for gustatory perception of dietary lipids.