Fatty acid oxidation and control of food intake
Fatty acid oxidation and control of food intake
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DOI：
10.1016/j.physbeh.2004.07.033
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发表时间：
2004-12-30
影响因子：
2.9
通讯作者：
Langhans, W
中科院分区：
文献类型：
--
作者：
Leonhardt, M;Langhans, W
脂肪酸氧化被认为在控制食物摄入中起作用，并且摄入的脂肪的低餐后氧化可能有助于高脂肪饮食中的暴饮暴食。脂肪酸氧化在控制食物摄入中的作用的证据主要来自于不同种属（大鼠、小鼠、人）对酰基辅酶A脱氢酶抑制剂巯基乙酸盐（MA）和其他脂肪酸氧化抑制剂给药的摄食刺激。去神经研究表明，这种“脂肪供给”与肝脏脂肪酸氧化的变化有关。与抑制脂肪酸氧化的摄食刺激作用的强有力的情况相反，刺激脂肪酸氧化的摄食抑制作用的证据是不一致的，并且相对较弱。摄入中链脂肪酸（MCFA）和外周给予已知会增加脂肪酸氧化的物质，例如脂肪酸合成酶抑制剂C75和β（3）-肾上腺素能激动剂，会减少进食。然而，这些物质也降低了大鼠对糖精溶液的通常偏好，表明摄食抑制作用不仅是由于脂肪酸氧化的刺激。一种可能的方法来回答这个问题是否刺激肝脂肪酸氧化增强饱腹感是选择性地增加表达和活性的酶CPT 1 α在肝脏。CPT 1alpha将细胞质中的长链脂肪酸从CoA转移到肉毒碱，这是长链脂肪酸进入线粒体的先决条件，也是线粒体脂肪酸氧化的速率控制步骤。诱导的，肝特异性过表达的CPT 1 α大鼠的产生应允许严格检查肝脂肪酸氧化控制食物摄入的假定贡献。(C)2004年爱思唯尔公司All rights reserved.
Fatty acid oxidation is thought to play a role in the control of food intake, and a low postprandial oxidation of ingested fat may contribute to the overeating on a high-fat diet. Evidence for a role of fatty acid oxidation in control of food intake is mainly derived from the stimulation of feeding in response to administration of the acyl-CoA-dehydrogenase inhibitor mercaptoacetate (MA) and other inhibitors of fatty acid oxidation in different species (rat, mouse, man). Denervation studies suggest that this "lipoprivic feedings" is related to changes in hepatic fatty acid oxidation. In contrast to the strong case for a feeding stimulatory effect of an inhibition of fatty acid oxidation, the evidence for a feeding suppressive effect of a stimulation of fatty acid oxidation is inconsistent and comparatively weak. Ingestion of medium-chain fatty acids (MCFA) and peripheral administration of substances known to increase fatty acid oxidation, such as the fatty acid synthase inhibitor C75 and beta(3)-adrenergic agonists, decrease feeding. Yet, these substances also reduce the rats' usual preference for saccharin solution, indicating that the feeding suppressive effect is not only due to a stimulation of fatty acid oxidation. A possible approach to answer the question of whether a stimulation of hepatic fatty acid oxidation enhances satiety is to selectively increase expression and activity of the enzyme CPT 1alpha in the liver. CPT 1alpha transfers long-chain fatty acids in the cytosol from CoA to carnitine, which is the precondition for the entry of long-chain fatty acids into mitochondria and the rate-controlling step in mitochondrial fatty acid oxidation. The generation of rats with inducible, liver-specific overexpression of CPT 1alpha should permit to critically examine the putative contribution of hepatic fatty acid oxidation to the control of food intake. (C) 2004 Elsevier Inc. All rights reserved.