Friedman M I
Monell Chemical Senses Center, Philadelphia, PA 19104.
Int J Obes. 1990;14 Suppl 3:53-66; discussion 66-7.
The role of body fat in the control of food intake is considered from the point of view that the oxidation of metabolic fuels generates a signal that governs feeding behavior. According to this perspective, the storage and mobilization of fat affect food intake indirectly by altering fuel oxidation. Hyperphagia during the development of obesity is thus treated as an appropriate response to a primary metabolic defect that causes fuels to be stored rather than oxidized. Evidence is presented that changes in insulin level and the activity of carnitine palmitoyltransferase I modulate feeding by altering the partitioning of fatty acids. The possibility that dietary interactions, acting through these mechanisms, may cause overeating of high-fat diets is discussed. It is proposed that the signal for feeding originates in the liver when both fatty acids and glucose are unavailable for oxidation.
从代谢燃料氧化产生控制进食行为的信号这一角度来考虑体脂在食物摄入控制中的作用。根据这一观点,脂肪的储存和动员通过改变燃料氧化间接影响食物摄入。因此,肥胖发展过程中的食欲亢进被视为对导致燃料储存而非氧化的原发性代谢缺陷的适当反应。有证据表明,胰岛素水平和肉碱棕榈酰转移酶I活性的变化通过改变脂肪酸的分配来调节进食。讨论了通过这些机制起作用的饮食相互作用可能导致高脂饮食过量进食的可能性。有人提出,当脂肪酸和葡萄糖都无法用于氧化时,进食信号起源于肝脏。