肥胖症和药物成瘾的常见细胞和分子机制。
Common cellular and molecular mechanisms in obesity and drug addiction.
机构信息
Laboratory of Behavioral and Molecular Neuroscience, Department of Molecular Therapeutics, The Scripps Research Institute Florida, 130 Scripps Way, Jupiter, Florida 33458, USA.
出版信息
Nat Rev Neurosci. 2011 Oct 20;12(11):638-51. doi: 10.1038/nrn3105.
The hedonic properties of food can stimulate feeding behaviour even when energy requirements have been met, contributing to weight gain and obesity. Similarly, the hedonic effects of drugs of abuse can motivate their excessive intake, culminating in addiction. Common brain substrates regulate the hedonic properties of palatable food and addictive drugs, and recent reports suggest that excessive consumption of food or drugs of abuse induces similar neuroadaptive responses in brain reward circuitries. Here, we review evidence suggesting that obesity and drug addiction may share common molecular, cellular and systems-level mechanisms.
食物的享乐特性即使在满足能量需求时也能刺激进食行为，导致体重增加和肥胖。同样，滥用药物的享乐效应也能促使人们过度摄入，最终导致成瘾。共同的大脑基质调节美味食物和成瘾药物的享乐特性，最近的报告表明，过量食用食物或滥用药物会在大脑奖励回路中引起类似的神经适应反应。在这里，我们回顾了一些证据，表明肥胖和药物成瘾可能具有共同的分子、细胞和系统水平的机制。
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