Norepinephrine- and epinephrine-deficient mice gain weight normally on a high-fat diet
Norepinephrine- and epinephrine-deficient mice gain weight normally on a high-fat diet
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DOI：
10.1038/oby.2005.185
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发表时间：
2005-09-01
期刊：
影响因子：
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通讯作者：
Palmiter, RD
中科院分区：
文献类型：
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作者：
Marie, LS;Luquet, S;Palmiter, RD
目的：去甲肾上腺素（NE）和肾上腺素（Epi）通过肾上腺素能受体（AR）的信号传导通过控制饮食诱导的产热来调节当小鼠被喂食高脂饮食（HFD）时的体重增加。因此，可以预测由于多巴胺β-羟化酶基因失活而不能产生NE/Epi的小鼠（Dbh缺失小鼠）将具有变得肥胖的倾向。我们的特点是响应Dbh-null和对照小鼠HFD.Research方法和程序：Dbh-null和对照小鼠喂食HFD或常规饮食（RD）2个月。测量体重、肥胖、肌肉甘油三酯水平和脂肪细胞大小，以及循环瘦素、脂联素、甘油三酯、葡萄糖和胰岛素水平。结果：Dbh基因敲除的小鼠在HFD上体重正常增加，并且具有相同的肥胖。他们的血清甘油三酯和瘦素水平正常，但脂肪细胞比对照组小30%。Dbh基因敲除小鼠在暴露于HFD时保持低血糖水平和葡萄糖耐量，与对照组相比。因为缺乏所有三种PARS的小鼠在HFD上变得肥胖，通过α-和PARS的信号传递的不平衡似乎是肥胖的原因。令人惊讶的是，Dbh缺失小鼠保持葡萄糖耐量。
Objective: Signaling through adrenergic receptors (ARs) by norepinephrine (NE) and epinephrine (Epi) regulates weight gain when mice are fed a high-fat diet (HFD) by controlling diet-induced thermogenesis. Thus, one would predict that mice unable to make NE/Epi because of inactivation of the dopamine beta-hydroxylase gene (Dbh-null mice) would have a propensity to become obese. We characterized the response of Dbh-null and control mice to a HFD.Research Methods and Procedures: Dbh-null and control mice were fed an HFD or a regular diet (RD) for 2 months. Body weight, adiposity, muscle triglyceride levels, and adipocyte size were measured, as were circulating leptin, adiponectin, triglyceride, glucose, and insulin levels. A glucose tolerance test was also preformed.Results: Dbh-null mice gain weight normally on an HFD and have the same adiposity. Their serum triglyceride and leptin levels are normal, but adipocytes are similar to 30% smaller than controls. Dbh-null mice maintain low blood glucose levels and glucose tolerance when exposed to the HFD in contrast to controls.Discussion: Complete lack of NE/Epi does not predispose to obesity. Because mice lacking all three PARS become obese on an HFD, an imbalance of signaling through alpha- and PARS seems to be responsible for obesity. Surprisingly, Dbh-null mice maintain glucose tolerance.