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人类肥胖:是脂质氧化缺陷还是产热缺陷?

Human obesity: a defect in lipid oxidation or in thermogenesis?

作者信息

Tremblay A

机构信息

Physical Activity Sciences Laboratory, PEPS, Laval University, Ste-Foy, Quebec, Canada.

出版信息

Int J Obes Relat Metab Disord. 1992 Dec;16(12):953-7.

PMID:1335974
Abstract

Numerous animal studies have shown that the development of obesity can depend on a decreased sympathetic nervous system activity but it has not been possible to convincingly demonstrate in humans that an excessive accumulation of adipose tissue might also be attributable to this factor. However, results from recent studies suggest that the contribution of the sympathetic nervous system to the development of human obesity may be greater than that generally believed by the scientific community. Indeed, experimental data show that the decrease in lipid oxidation induced by beta adrenergic blockade under free living conditions is substantially higher than the decrease in energy expenditure. Moreover, there are individual variations in the relative capacity to use lipid as an energy substrate under standardized conditions of diet composition. If the contribution of lipid to daily energy expenditure is reduced, there are two options to reach energy balance if physical activity habits are not modified. The first possibility is reduction in the relative lipid content of the diet to match the lipid content of the fuel mix oxidized. The second option is a gain in body weight and fat until the associated increase in the lipid content of the substrate mix is sufficient to re-equilibrate substrate and energy balance. Under high fat diet conditions, this gain in body weight and fat can be large enough to lead to an obese state. As described in this report, an integration of these observations suggests that further research pertaining to the role of sympathetic nervous system activity in human obesity should be focused as much on lipid oxidation as on thermogenesis.

摘要

众多动物研究表明,肥胖的发展可能取决于交感神经系统活动的降低,但在人类中尚未能够令人信服地证明脂肪组织的过度积累也可能归因于这一因素。然而,最近的研究结果表明,交感神经系统对人类肥胖发展的贡献可能比科学界普遍认为的更大。事实上,实验数据表明,在自由生活条件下,β肾上腺素能阻断引起的脂质氧化减少幅度远高于能量消耗的减少幅度。此外,在饮食组成标准化的条件下,个体在将脂质用作能量底物的相对能力方面存在差异。如果脂质对每日能量消耗的贡献减少,而体力活动习惯又未改变,那么有两种选择来实现能量平衡。第一种可能性是减少饮食中的相对脂质含量,以使其与氧化的燃料混合物中的脂质含量相匹配。第二种选择是体重和脂肪增加,直到底物混合物中脂质含量的相应增加足以重新平衡底物和能量平衡。在高脂肪饮食条件下,这种体重和脂肪的增加可能会大到足以导致肥胖状态。如本报告所述,综合这些观察结果表明,关于交感神经系统活动在人类肥胖中的作用的进一步研究应同样关注脂质氧化和产热。

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Human obesity: a defect in lipid oxidation or in thermogenesis?人类肥胖:是脂质氧化缺陷还是产热缺陷?
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Thermogenesis in human brown adipose tissue and skeletal muscle induced by sympathomimetic stimulation.拟交感神经刺激诱导的人体棕色脂肪组织和骨骼肌产热。
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Diet-induced thermogenesis and substrate oxidation are not different between lean and obese women after two different isocaloric meals, one rich in protein and one rich in fat.在食用两种不同的等热量餐食(一种富含蛋白质,一种富含脂肪)后,瘦女性和肥胖女性之间的饮食诱导产热和底物氧化并无差异。
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