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味觉感知膳食脂肪的细胞信号机制:进展与挑战。

Cell signaling mechanisms of oro-gustatory detection of dietary fat: advances and challenges.

机构信息

Department of Biology, Utah State University, 5305 Old Main Hill, Logan, UT 84322, USA.

INSERM U866, Université de Bourgogne/AgroSup, Dijon 2100, France.

出版信息

Prog Lipid Res. 2014 Jan;53:82-92. doi: 10.1016/j.plipres.2013.11.001. Epub 2013 Nov 21.

DOI:10.1016/j.plipres.2013.11.001
PMID:24269201
Abstract

CD36 and two G-protein coupled receptors (GPCR), i.e., GPR120 and GPR40, have been implicated in the gustatory perception of dietary fats in rodents. These glycoproteins are coupled to increases in free intracellular Ca²⁺ concentrations, Ca²⁺, during their activation by dietary long-chain fatty acids (LCFA). The transient receptor potential type M5 (TRPM5) channel, activated by Ca²⁺, participates in downstream signaling in taste bud cells (TBC). The mice, knocked-out for expression of CD36, GPR120, GPR40 or TRPM5 have a reduced spontaneous preference for fat. The delayed rectifying K⁺ (DRK) channels believed to lie downstream of these receptors are also important players in fat taste transduction. The trigeminal neurons by triggering increases in Ca²⁺ may influence the taste signal to afferent nerve fibers. Why are there so many taste receptor candidates for one taste modality? We discuss the recent advances on the role of CD36, GPR120, GPR40, TRPM5 and DRK channels, in signal transduction in TBC. We shed light on their cross-talk and delineate their roles in obesity as a better understanding of the molecular mechanisms behind their regulation could eventually lead to new strategies to fight against this condition.

摘要

CD36 和两种 G 蛋白偶联受体(GPCR),即 GPR120 和 GPR40,已被牵连到啮齿动物对膳食脂肪的味觉感知中。这些糖蛋白在其被膳食长链脂肪酸(LCFA)激活时,与细胞内游离 Ca²⁺浓度 (Ca²⁺) 的增加偶联。瞬时受体电位型 M5 (TRPM5) 通道,被 Ca²⁺ 激活,参与味觉感受器细胞(TBC)中的下游信号转导。CD36、GPR120、GPR40 或 TRPM5 表达缺失的小鼠对脂肪的自发偏好降低。被认为位于这些受体下游的延迟整流钾 (DRK) 通道也是脂肪味觉转导中的重要参与者。三叉神经神经元通过触发 Ca²⁺ 的增加,可能会影响传入神经纤维的味觉信号。为什么一种味觉模式会有如此多的味觉受体候选者?我们讨论了 CD36、GPR120、GPR40、TRPM5 和 DRK 通道在 TBC 中的信号转导中的最新进展。我们阐明了它们的串扰,并描述了它们在肥胖中的作用,因为更好地理解其调节背后的分子机制最终可能会导致对抗这种疾病的新策略。

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