CD36- and GPR120-mediated Ca²⁺ signaling in human taste bud cells mediates differential responses to fatty acids and is altered in obese mice.
CD36- and GPR120-mediated Ca²⁺ signaling in human taste bud cells mediates differential responses to fatty acids and is altered in obese mice.
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DOI：
10.1053/j.gastro.2014.01.006
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发表时间：
2014-04
期刊：
影响因子：
29.4
通讯作者：
Khan NA
中科院分区：
文献类型：
--
作者：
Ozdener MH;Subramaniam S;Sundaresan S;Sery O;Hashimoto T;Asakawa Y;Besnard P;Abumrad NA;Khan NA
增加我们对味觉检测膳食脂肪及其对脂肪偏好的贡献的了解是很重要的。我们研究了脂肪味觉受体CD36和GPR120在真菌样味蕾细胞(TBC)中的作用以及它们之间通过钙信号的相互作用。我们检测了小干扰RNA(SiRNAs)对编码CD36和GPR120的mRNAs(或对照siRNAs)的影响。我们还研究了CD36−/−小鼠、野生型瘦小鼠和肥胖小鼠外周血中的钙信号。此外，还对表达GPR120并稳定转染人CD36的小鼠肠内分泌细胞株STC-1进行了研究。我们测量了CD36和GPR120激活后人和小鼠TBC释放的5-羟色胺和GLP-1。高浓度亚油酸通过CD36和GPR120诱导人和小鼠TBC以及STC-1细胞的钙信号转导，而低浓度亚油酸仅通过CD36诱导钙信号转导。去甲油酸与人和小鼠菌样TBC孵育后，膜脂筏CD36表达下调，GPR120表达上调。肥胖小鼠对脂肪的自发偏好降低。来自肥胖小鼠的菌状TBC降低了钙离子和5-羟色胺的反应，但增加了GLP1的释放，并降低了脂筏中CD36的水平，增加了GPR120的水平。CD36和GPR120在味觉感知膳食脂肪的TBC信号中具有不重叠的作用；它们受到肥胖的不同调节。
It is important to increase our understanding of gustatory detection of dietary fat and its contribution to fat preference. We studied the roles of the fat taste receptors CD36 and GPR120 and their interactions via Ca2+ signaling in fungiform taste bud cells (TBC). We measured Ca2+ signaling in human TBC, transfected with small interfering RNAs (siRNAs) against mRNAs encoding CD36 and GPR120 (or control siRNAs). We also studied Ca2+ signaling in TBC from CD36−/− mice and from wild-type lean and obese mice. Additional studies were conducted with mouse enteroendocrine cell line STC-1 that express GPR120 and stably transfected with human CD36. We measured release of serotonin and GLP-1 from human and mice TBC in response to CD36 and GPR120 activation. High concentrations of linoleic acid induced Ca2+ signaling via CD36 and GPR120 in human and mice TBC as well as in STC-1 cells, whereas low concentrations induced Ca2+ signaling via only CD36. Incubation of human and mice fungiform TBC with lineoleic acid downregulated CD36 and upregulated GPR120 in membrane lipid rafts. Obese mice had decreased spontaneous preference for fat. Fungiform TBC from obese mice had reduced Ca2+ and serotonin responses but increased release of GLP1, along with reduced levels of CD36 and increased levels of GPR120 in lipid rafts. CD36 and GPR120 have non-overlapping roles in TBC signaling during oro-gustatory perception of dietary lipids; these are differentially regulated by obesity.
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