The role of T1r3 and Trpm5 in carbohydrate-induced obesity in mice.
The role of T1r3 and Trpm5 in carbohydrate-induced obesity in mice.
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DOI：
10.1016/j.physbeh.2012.05.023
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发表时间：
2012-08-20
影响因子：
2.9
通讯作者：
Sclafani A
中科院分区：
文献类型：
--
作者：
Glendinning JI;Gillman J;Zamer H;Margolskee RF;Sclafani A
我们研究了T1 r3和Trpm 5味觉信号蛋白在碳水化合物诱导的暴饮暴食和肥胖中的作用。T1 r3由Tas 1 r3编码，是T1 r2 + T1 r3糖味觉受体的一部分，而Trpm 5介导味觉细胞中G蛋白偶联受体的信号传导。已知C57 BL/6野生型（WT）和Tas 1 r3基因敲除（KO）小鼠被多糖（一种葡萄糖聚合物）的味道所吸引，而不是蔗糖。相比之下，Trpm 5 KO小鼠不被蔗糖或多糖的味道所吸引。在实验1中，我们将WT、Tas 1 r3 KO和Trpm 5 KO小鼠维持在三种饮食中的一种38天：实验室食物加水（对照饮食）;食物、水和34%多糖溶液（多糖饮食）;或食物、水和34%蔗糖溶液（蔗糖饮食）。WT和Tas 1 r3 KO小鼠过度食用多糖饮食并变得肥胖。WT和Tas 1 r3 KO小鼠也过度食用蔗糖饮食，但只有WT小鼠变得肥胖。相比之下，Trpm 5 KO小鼠在蔗糖和多糖饮食中表现出很少或没有暴饮暴食，并且在这些饮食中体重增加略低于或显著低于WT小鼠。在实验2中，我们询问Tas 1 r3 KO小鼠在蔗糖饮食中是否表现出体重增加受损，因为它是无味的。为了检验这一假设，我们将WT和Tas 1 r3 KO小鼠维持在两种饮食之一38天：食物、水和稀释的（1%）但非常可口的Intraperoid乳剂（对照饮食）;或食物、水和34%蔗糖+1% Intraperoid溶液（Suc+IL饮食）。WT和Tas 1 r3 KO小鼠在Suc+IL饮食中体重增加并变得肥胖。我们的研究结果表明，营养液必须非常可口，才能引起小鼠碳水化合物诱导的肥胖，而可口性部分通过提高营养利用率来产生这种效果。
We examined the role of T1r3 and Trpm5 taste signaling proteins in carbohydrate-induced overeating and obesity. T1r3, encoded by Tas1r3, is part of the T1r2+T1r3 sugar taste receptor, while Trpm5 mediates signaling for G protein-coupled receptors in taste cells. It is known that C57BL/6 wild-type (WT) and Tas1r3 knock-out (KO) mice are attracted to the taste of Polycose (a glucose polymer), but not sucrose. In contrast, Trpm5 KO mice are not attracted to the taste of sucrose or Polycose. In Experiment 1, we maintained the WT, Tas1r3 KO and Trpm5 KO mice on one of three diets for 38 days: lab chow plus water (Control diet); chow, water and 34% Polycose solution (Polycose diet); or chow, water and 34% sucrose solution (Sucrose diet). The WT and Tas1r3 KO mice overconsumed the Polycose diet and became obese. The WT and Tas1r3 KO mice also overconsumed the Sucrose diet, but only the WT mice became obese. The Trpm5 KO mice, in contrast, showed little or no overeating on the Sucrose and Polycose diets, and gained slightly or significantly less weight than WT mice on these diets. In Experiment 2, we asked whether the Tas1r3 KO mice exhibited impaired weight gain on the Sucrose diet because it was insipid. To test this hypothesis, we maintained the WT and Tas1r3 KO mice on one of two diets for 38 days: chow, water and a dilute (1%) but highly palatable Intralipid emulsion (Control diet); or chow, water and a 34% sucrose + 1% Intralipid solution (Suc+IL diet). The WT and Tas1r3 KO mice both gained weight and became obese on the Suc+IL diet. Our results suggest that nutritive solutions must be highly palatable to cause carbohydrate-induced obesity in mice, and that palatability produces this effect in part by enhancing nutrient utilization.
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DOI：
10.1007/s00424-010-0835-z
发表时间：
2010-06
期刊：
Pflugers Archiv : European journal of physiology
影响因子：
--
作者：
Brixel LR;Monteilh-Zoller MK;Ingenbrandt CS;Fleig A;Penner R;Enklaar T;Zabel BU;Prawitt D
通讯作者：
Prawitt D
影响因子：
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作者：
Drewnowski, A
通讯作者：
Drewnowski, A
DOI：
10.1038/oby.2005.136
发表时间：
2005-07-01
期刊：
OBESITY RESEARCH
影响因子：
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作者：
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通讯作者：
Tschöp, MH
影响因子：
2.9
作者：
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通讯作者：
Malik, Vasanti S.
影响因子：
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作者：
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