βAR signaling required for diet-induced thermogenesis and obesity resistance
βAR signaling required for diet-induced thermogenesis and obesity resistance
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DOI：
10.1126/science.1073160
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发表时间：
2002-08-02
期刊：
影响因子：
56.9
通讯作者：
Lowell, BB
中科院分区：
文献类型：
--
作者：
Bachman, ES;Dhillon, H;Lowell, BB
过量的热量摄入被认为是由大脑感知的，然后激活产热作为预防肥胖的一种手段。交感神经系统通过β-肾上腺素能受体（β AR）作用于靶组织，可能是这种稳态机制的传出臂。为了验证这一假设，我们创造了缺乏三种已知β AR的小鼠（无β AR小鼠）。吃普通饲料的β-较少的小鼠具有降低的代谢率并且轻微肥胖。在高脂肪饮食中，与野生型小鼠相比，β-较少的小鼠发展出大量肥胖，这完全是由于饮食诱导的产热失败。这些发现证实了β AR是饮食诱导的产热所必需的，并且这种传出途径在身体防御饮食诱导的肥胖中起着关键作用。
Excessive caloric intake is thought to be sensed by the brain, which then activates thermogenesis as a means of preventing obesity. The sympathetic nervous system, through beta-adrenergic receptor (betaAR) action on target tissues, is likely the efferent arm of this homeostatic mechanism. To test this hypothesis, we created mice that lack the three known betaARs (beta-less mice). beta-less mice on a Chow diet had a reduced metabolic rate and were slightly obese. On a high-fat diet, beta-less mice, in contrast to wild-type mice, developed massive obesity that was due entirely to a failure of diet-induced thermogenesis. These findings establish that betaARs are necessary for diet-induced thermogenesis and that this efferent pathway plays a critical role in the body's defense against diet-induced obesity.