Department of Biology, Utah State University, Logan, Utah 84322, USA.
J Neurosci. 2011 Jun 8;31(23):8634-42. doi: 10.1523/JNEUROSCI.6273-10.2011.
Until recently, dietary fat was considered to be tasteless, and its primary sensory attribute was believed to be its texture (Rolls et al., 1999; Verhagen et al., 2003). 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 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.
直到最近,人们还认为脂肪没有味道,其主要感官属性被认为是质地(Rolls 等人,1999 年;Verhagen 等人,2003 年)。然而,许多研究已经证明了脂肪成分,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,我们首次表明,长链不饱和游离脂肪酸亚油酸(LA)通过激活瞬时受体电位通道型 M5(TRPM5)使小鼠味觉细胞去极化,并引发强烈的细胞内钙升高。LA 诱导的反应取决于 G 蛋白-磷脂酶 C 途径,表明 G 蛋白偶联受体(GPCR)参与了脂肪酸的转导。缺乏 TRPM5 通道的小鼠对 LA 没有偏好,且对 LA 的敏感性降低。总之,这些研究表明,TRPM5 通道在小鼠味觉细胞中脂肪酸转导中发挥着重要作用,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。