Houmard Joseph A
Human Performance Laboratory, Department of Exercise and Sport Science, East Carolina University, Greenville, North Carolina 27858, USA.
Am J Physiol Regul Integr Comp Physiol. 2008 Apr;294(4):R1111-6. doi: 10.1152/ajpregu.00396.2007. Epub 2008 Feb 6.
There is an accumulating amount of evidence indicating that lipid oxidation is depressed in the skeletal muscle of obese individuals. Decrements in fatty acid oxidation (FAO) have been reported with obesity in models ranging from whole body measurements to isolated skeletal muscle preparations as well as in myotubes raised in culture. This reduction appears to be associated with a depression in the activities of enzymes involved in various steps of lipid oxidation, which subsequently partitions lipid entering the cell toward storage. The defect in FAO in skeletal muscle may be critical in relation to health, as a reduction in the capacity for lipid oxidation could directly or indirectly contribute to the insulin resistance commonly evident with obesity. Although less characterized, a decrement in FAO has also been linked with weight gain, which suggests that this characteristic may be an integral aspect leading to the obese state. In terms of intervention, weight loss does not seem to correct the defect in FAO with obesity. This review will provide evidence supporting a reduction in muscle FAO with obesity.
越来越多的证据表明,肥胖个体的骨骼肌中脂质氧化受到抑制。从全身测量到分离的骨骼肌制剂,以及在培养中培养的肌管等模型中,均已报道肥胖会导致脂肪酸氧化(FAO)减少。这种减少似乎与脂质氧化各个步骤中涉及的酶活性降低有关,这随后使进入细胞的脂质转向储存。骨骼肌中FAO的缺陷可能对健康至关重要,因为脂质氧化能力的降低可能直接或间接导致肥胖常见的胰岛素抵抗。虽然对其特征描述较少,但FAO的减少也与体重增加有关,这表明这一特征可能是导致肥胖状态的一个不可或缺的方面。在干预方面,体重减轻似乎并不能纠正肥胖导致的FAO缺陷。本综述将提供证据支持肥胖会导致肌肉FAO减少。