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 Ca 2+ depletion in the endoplasmic reticulum, mediates fatty acid-induced Ca 2+ 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 A 2 isoforms via CD36. This activation triggered Ca 2+ influx in CD36-positive taste bud cells (TBCs) purified from mouse CVP. LA also induced the production of Ca 2+ influx factor (CIF). STIM1 was found to regulate LA-induced CIF production and the opening of multiple store-operated Ca 2+ (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 Ca 2+ signaling, regulated by STIM1 via CD36, might be implicated in oro-gustatory perception of dietary lipids and the spontaneous preference for fat. IntroductionThe sense of taste informs the organism about the quality of ingested food. Five basic taste modalities, e.g., sweet, sour, bitter, salty, and umami, have so far been identified (1). Recent compelling evidence from rodents raises the possibility of an additional sixth taste modality devoted to the perception of lipids (2-4) that are released by the action of lingual lipases, present in the salivary secretions (5). Fukuwatari et al. (6) and Laugerette et al. (2) have documented the expression of the receptor-like lipid-binding protein CD36 in rat and mouse circumvallate papillae (CVP), respectively. Laugerette et al. (2) have provided the first evidence for the involvement of lingual CD36 in dietary lipid perception in the mouse. Indeed, Cd36 gene inactivation completely abolished the spontaneous preference for long-chain fatty acids (LCFAs) observed in wild-type mice. This effect is lipid specific, since the preference for sweet and aversion to bitterness reported in controls were not altered in Cd36-null mice. These observations regarding the implication of CD36 in the perception of lipid taste have also been confirmed by other investigators (7).The coupling of CD36 cell signaling to a downstream second messenger cascade has been explored in mouse taste bud cells (TBCs) (3,8). The experiments conducted on CD36-positive TBCs purified from mouse CVP demonstrated that linoleic acid (LA), an LCFA, induced increases in free intracellular calcium concentrations, [Ca 2+ ] i by binding to CD36 (3). We have reported that LCFAs induced the production of inositol-1,4,5-trisphosphate (IP 3 ) and, consequently, recruited Ca 2+ from the endoplasmic reticulum, followed by Ca 2+ inf...

Zizyphus lotus, belonging to the Rhamnaceae family, is a deciduous shrub which generally grows in arid and semiarid regions of the globe. In traditional medicine, Z. lotus is used as antidiabetes, sedative, bronchitis, and antidiarrhea by local populations. Recently, several scientific reports for health benefit and nutritional potential of bioactive compounds from this jujube have been reported. This plant is rich in polyphenols, cyclopeptide alkaloids, dammarane saponins, vitamins, minerals, amino acids, and polyunsaturated fatty acids. These identified compounds were supposed to be responsible for most of Z. lotus biologically relevant activities including antimicrobial, anti-inflammatory, hypoglycemic, antioxidant, and immunomodulatory effects. The aim of the present review was to give particular emphasis on the most recent findings on biological effects of the major groups of Zizyphus lotus components and their medical interest, notably for human nutrition, health benefit, and therapeutic impacts.

A relationship between orosensory detection of dietary lipids, regulation of fat intake, and body mass index was recently suggested. However, involved mechanisms are poorly understood. Moreover, whether obesity can directly modulate preference for fatty foods remains unknown. To address this question, exploration of the oral lipid sensing system was undertaken in diet-induced obese (DIO) mice. By using a combination of biochemical, physiological, and behavioral approaches, we found that i) the attraction for lipids is decreased in obese mice, ii) this behavioral change has an orosensory origin, iii) it is reversed in calorie-restricted DIO mice, revealing an inverse correlation between fat preference and adipose tissue size, iv) obesity suppresses the lipid-mediated downregulation of the lipid-sensor CD36 in circumvallate papillae, usually found during the refeeding of lean mice, and v) the CD36-dependent signaling cascade controlling the intracellular calcium levels ([Ca2+]i) in taste bud cells is decreased in obese mice. Therefore, obesity alters the lipid-sensing system responsible for the oral perception of dietary lipids. This phenomenon seems to take place through a CD36-mediated mechanism, leading to changes in eating behavior.

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