Transient receptor potential channel type M5 is essential for fat taste.
Transient receptor potential channel type M5 is essential for fat taste.
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DOI：
10.1523/jneurosci.6273-10.2011
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发表时间：
2011-06-08
期刊：
影响因子：
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通讯作者：
Gilbertson TA
中科院分区：
文献类型：
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作者：
Liu P;Shah BP;Croasdell S;Gilbertson TA
直到最近，膳食脂肪被认为是无味的，其主要感官属性被认为是其质地。然而，许多研究已经证明了脂肪中的成分，特别是游离脂肪酸，能够激活味觉细胞并引发与脂肪味道一致的行为反应。在这里，我们第一次表明，长链不饱和游离脂肪酸，亚油酸（LA），去极化小鼠味觉细胞，并通过激活瞬时受体电位通道类型M5（TRPM 5），eliminates一个强大的细胞内钙上升。LA诱导的反应依赖于G蛋白-磷脂酶C（PLC）途径，表明G蛋白偶联受体（GPCR）参与脂肪酸的转导。缺乏TRPM 5通道的小鼠表现出对LA没有偏好，并且表现出对LA的敏感性降低。总之，这些研究表明，TRPM 5通道在小鼠味觉细胞中的脂肪酸转导中发挥重要作用，并表明脂肪酸能够以与其他GPCR介导的味觉一致的方式激活味觉细胞。
Until recently, dietary fat was considered to be tasteless and its primary sensory attribute was believed to be its texture. However, a number of studies have demonstrated the ability of components in fats, specifically free fatty acids, to activate taste cells and elicit behavioral responses consistent with there being a taste of fat. Here we show for the first time that long chain unsaturated free fatty acid, linoleic acid (LA), depolarizes mouse taste cells and elicits a robust intracellular calcium rise via the activation of transient receptor potential channel type M5 (TRPM5). The LA-induced responses depend on G protein-phospholipase C (PLC) pathway indicative of the involvement of G protein-coupled receptors (GPCRs) in the transduction of fatty acids. Mice lacking TRPM5 channels exhibit no preference for and show reduced sensitivity to LA. Together, these studies show that TRPM5 channels play an essential role in fatty acid transduction in mouse taste cells and suggest that fatty acids are capable of activating taste cells in a manner consistent with other GPCR-mediated tastes.