Bosy-Westphal A, Hägele F, Nas A
Institut für Ernährungsmedizin, Angewandte Ernährungswissenschaft, Universität Hohenheim, Stuttgart, Germany.
Eur J Clin Nutr. 2017 Mar;71(3):327-330. doi: 10.1038/ejcn.2016.230. Epub 2016 Nov 30.
The 'carbohydrate-insulin theory of obesity' is used to justify popular health claims stating that carbohydrates make you fat or a high glycemic load and consumption of sugar-sweetened beverages (SSBs) and breakfast skipping increase fat gain. According to this theory, the elevated postprandial insulin secretion to a high glycemic challenge is blamed as a causal mechanism by directing nutrients away from oxidation in muscle towards storage in adipose tissue. Scientific evidence is however largely disagreeing with an adverse effect of postprandial hyperinsulinemia on fuel partitioning. Possible reasons for this disagreement are differences in insulin sensitivity and energy balance. Diet-induced hyperinsulinemia may lead to a higher fat storage only at a positive energy balance. A shift in fuel partitioning towards fat storage requires improved or maintained insulin sensitivity in adipose tissue when compared with skeletal muscle. This may be the case during refeeding (after weight loss), physical inactivity or in metabolically healthy obese subjects (relative to insulin-resistant subjects). The adverse effect of a high-glycemic diet, SSBs consumption or breakfast skipping on body weight is likely due to increased energy consumption rather than to increased fat storage.
“肥胖的碳水化合物-胰岛素理论”被用来为一些流行的健康观点提供依据,这些观点认为碳水化合物会使人发胖,或者高血糖负荷以及饮用含糖饮料(SSB)和不吃早餐会增加脂肪堆积。根据这一理论,餐后胰岛素分泌因高血糖刺激而升高,被认为是一种因果机制,它会使营养物质从肌肉氧化转向脂肪组织储存。然而,科学证据在很大程度上并不认同餐后高胰岛素血症对燃料分配有不良影响。这种分歧的可能原因在于胰岛素敏感性和能量平衡的差异。饮食诱导的高胰岛素血症可能仅在能量平衡为正时导致更高的脂肪储存。与骨骼肌相比,当脂肪组织中的胰岛素敏感性得到改善或维持时,燃料分配向脂肪储存的转变才可能发生。这种情况可能发生在重新进食(体重减轻后)、身体不活动或代谢健康的肥胖受试者(相对于胰岛素抵抗受试者)身上。高糖饮食、饮用含糖饮料或不吃早餐对体重的不良影响可能是由于能量消耗增加,而非脂肪储存增加。