Faculty of Biology and Medicine, Department of Physiology, University of Lausanne, Lausanne, Switzerland.
Int J Obes (Lond). 2016 Mar;40 Suppl 1:S28-9. doi: 10.1038/ijo.2016.11.
In this closing perspective, the author exposes why targeting a single nutrient like sugar is in his opinion unlikely to be efficient in preventing obesity and metabolic diseases. He defends the proposal that the concept of fructose toxicity is based on major misconceptions of nutritional physiology. He specifically proposes that (1) sugar being a non-essential nutrient does not obligatorily imply that it has no beneficial effect; (2) alterations of blood triglyceride concentration and hepatic glucose production within the normal range may merely reflect adaptations to a fructose-rich diet rather than early markers of diseases; (3) overfeeding is a normal physiological response to exposure to an energy-dense, palatable nutrient rather than the consequence of 'leptin resistance'; (4) we may presently overemphasize the role of biological regulations and of gene-related heredity when assessing the effects of fructose in particular, and the determinants of obesity in general.
在这篇结束性的观点文章中,作者揭示了为什么针对单一营养素(如糖)不太可能有效预防肥胖和代谢疾病。他认为果糖毒性的概念基于营养生理学的重大误解。他特别提出:(1)糖作为非必需营养素,并不一定意味着它没有有益的效果;(2)在正常范围内,血液三酰甘油浓度和肝葡萄糖生成的改变可能仅仅反映了对富含果糖饮食的适应,而不是疾病的早期标志物;(3)过度喂养是对摄入高热量、美味营养物质的正常生理反应,而不是“瘦素抵抗”的后果;(4)在评估果糖的作用,特别是肥胖的决定因素时,我们可能过于强调生物调节和与基因相关的遗传的作用。