Impact of obesity on taste receptor expression in extra-oral tissues: emphasis on hypothalamus and brainstem.
Impact of obesity on taste receptor expression in extra-oral tissues: emphasis on hypothalamus and brainstem.
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DOI：
10.1038/srep29094
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发表时间：
2016-07-08
影响因子：
4.6
通讯作者：
Aerts JM
中科院分区：
文献类型：
--
作者：
Herrera Moro Chao D;Argmann C;Van Eijk M;Boot RG;Ottenhoff R;Van Roomen C;Foppen E;Siljee JE;Unmehopa UA;Kalsbeek A;Aerts JM
甜的感觉会促进食物的摄入，而苦的感觉则会抑制食物的摄入。令人惊讶的是，在瘦小鼠和肥胖小鼠的口腔和口腔外组织中，甜味G蛋白偶联味觉受体（GPCTR）亚基（T1R2和T1R3）和苦味GPCTR （T2R116、T2R118、T2R138和T2R104）以及相关信号复合物α-亚基（αGustducin、Gα14和αTransducin）的表达仍然缺乏特征。我们关注肥胖对参与能量稳态的大脑区域（即下丘脑和脑干）味觉受体表达的影响。我们发现许多GPCTRs和α-亚基在这些组织中共表达，肥胖降低了T1R3、T2R116、Gα14、αTrans和TRPM5的表达。体外高水平葡萄糖诱导培养的下丘脑神经元细胞T1R2和g - α14表达显著下调，瘦素诱导T1R2和T1R3表达短暂下调。有趣的是，在瘦老鼠和肥胖老鼠的其他口腔外组织中也观察到表达差异，最显著的是在十二指肠，肥胖减少了大多数苦味和甜味受体的表达。综上所述，肥胖影响了十二指肠的甜味和苦味感知成分以及小鼠大脑中参与能量稳态的区域，包括下丘脑和脑干。
Sweet perception promotes food intake, whereas that of bitterness is inhibitory. Surprisingly, the expression of sweet G protein-coupled taste receptor (GPCTR) subunits (T1R2 and T1R3) and bitter GPCTRs (T2R116, T2R118, T2R138 and T2R104), as well as the α-subunits of the associated signalling complex (αGustducin, Gα14 and αTransducin), in oral and extra-oral tissues from lean and obese mice, remains poorly characterized. We focused on the impact of obesity on taste receptor expression in brain areas involved in energy homeostasis, namely the hypothalamus and brainstem. We demonstrate that many of the GPCTRs and α-subunits are co-expressed in these tissues and that obesity decreases expression of T1R3, T2R116, Gα14, αTrans and TRPM5. In vitro high levels of glucose caused a prominent down-regulation of T1R2 and Gα14 expression in cultured hypothalamic neuronal cells, leptin caused a transient down-regulation of T1R2 and T1R3 expression. Intriguingly, expression differences were also observed in other extra-oral tissues of lean and obese mice, most strikingly in the duodenum where obesity reduced the expression of most bitter and sweet receptors. In conclusion, obesity influences components of sweet and bitter taste sensing in the duodenum as well as regions of the mouse brain involved in energy homeostasis, including hypothalamus and brainstem.