丁酰胆碱酯酶基因敲除小鼠在高脂饮食下会肥胖。
The butyrylcholinesterase knockout mouse is obese on a high-fat diet.
作者信息
Li Bin, Duysen Ellen G, Lockridge Oksana
机构信息
Eppley Institute, University of Nebraska Medical Center, 986805 Nebraska Medical Center, Omaha, NE 68198-6805, USA.
出版信息
Chem Biol Interact. 2008 Sep 25;175(1-3):88-91. doi: 10.1016/j.cbi.2008.03.009. Epub 2008 Mar 22.
Butyrylcholinesterase (BChE) inactivates the appetite stimulating hormone octanoyl-ghrelin. The hypothesis was tested that BChE-/- mice would have abnormally high body weight and high levels of octanoyl-ghrelin. It was found that BChE-/- mice fed a standard 5% fat diet had normal body weight. However, BChE-/- mice fed a diet containing 11% fat became obese. Their obesity was not explained by increased levels of octanoyl-ghrelin, or by increased caloric intake, or by decreased exercise. Instead, a role for BChE in fat utilization was suggested.
丁酰胆碱酯酶（BChE）可使食欲刺激激素辛酰基胃饥饿素失活。研究人员对“BChE基因敲除小鼠体重异常高且辛酰基胃饥饿素水平高”这一假设进行了验证。结果发现，喂食标准5%脂肪饮食的BChE基因敲除小鼠体重正常。然而，喂食含11%脂肪饮食的BChE基因敲除小鼠变得肥胖。它们的肥胖并非由辛酰基胃饥饿素水平升高、热量摄入增加或运动量减少所致。相反，这表明BChE在脂肪利用中发挥作用。
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