Wolever T M
Department of Nutritional Sciences, Faculty of Medicine, University of Toronto, Canada.
Br J Nutr. 2000 Mar;83 Suppl 1:S97-102. doi: 10.1017/s0007114500001021.
The metabolic syndrome represents a vicious cycle whereby insulin resistance leads to compensatory hyperinsulinaemia, which maintains normal plasma glucose but may exacerbate insulin resistance. Excess insulin secretion may eventually reduce beta-cell function due to amyloid deposition, leading to raised blood glucose and further deterioration of beta-cell function and insulin sensitivity via glucose toxicity. Reducing postprandial glucose and insulin responses may be a way to interrupt this process, but there is disagreement about the dietary approach to achieve this. Glucose and insulin responses are determined primarily by the amount of carbohydrate consumed and its rate of absorption. Slowly absorbed, low glycaemic-index (GI) foods are associated with increased HDL cholesterol and reduced risk of type 2 diabetes. There is some evidence that low-GI foods improve insulin sensitivity in humans, although studies using established techniques (glucose clamp or frequently sampled intravenous glucose tolerance test) have not been done. Low carbohydrate diets have been suggested to be beneficial in the treatment of the metabolic syndrome because of reduced postprandial insulin. However, they may increase fasting glucose and impair oral glucose tolerance--effects which define carbohydrate intolerance. The effects of low carbohydrate diets on insulin sensitivity depend on what is used to replace the dietary carbohydrate, and the nature of the subjects studied. Dietary carbohydrates may affect insulin action, at least in part, via alterations in plasma free fatty acids. In normal subjects a high-carbohydrate/low-GI breakfast meal reduced free fatty acids by reducing the undershoot of plasma glucose, whereas low-carbohydrate breakfasts increased postprandial free fatty acids. It is unknown if these effects occur in insulin-resistant or diabetic subjects. Thus further work needs to be done before a firm conclusion can be drawn as to the optimal amount and type of dietary carbohydrate for the treatment of the metabolic syndrome.
代谢综合征代表了一个恶性循环,即胰岛素抵抗导致代偿性高胰岛素血症,后者维持血浆葡萄糖正常,但可能会加剧胰岛素抵抗。胰岛素分泌过多最终可能因淀粉样蛋白沉积而降低β细胞功能,导致血糖升高,并通过葡萄糖毒性使β细胞功能和胰岛素敏感性进一步恶化。降低餐后血糖和胰岛素反应可能是中断这一过程的一种方法,但对于实现这一目标的饮食方法存在分歧。葡萄糖和胰岛素反应主要由摄入的碳水化合物量及其吸收速度决定。缓慢吸收的低血糖指数(GI)食物与高密度脂蛋白胆固醇增加以及2型糖尿病风险降低有关。有一些证据表明,低GI食物可改善人体的胰岛素敏感性,尽管尚未使用既定技术(葡萄糖钳夹或频繁采样静脉葡萄糖耐量试验)进行研究。由于餐后胰岛素减少,低碳水化合物饮食已被认为对代谢综合征的治疗有益。然而,它们可能会增加空腹血糖并损害口服葡萄糖耐量,这些效应定义了碳水化合物不耐受。低碳水化合物饮食对胰岛素敏感性的影响取决于用于替代膳食碳水化合物的物质以及所研究受试者的性质。膳食碳水化合物可能至少部分通过血浆游离脂肪酸的改变来影响胰岛素作用。在正常受试者中,高碳水化合物/低GI早餐通过减少血糖下降来降低游离脂肪酸,而低碳水化合物早餐则增加餐后游离脂肪酸。尚不清楚这些效应是否发生在胰岛素抵抗或糖尿病患者中。因此,在就治疗代谢综合征的最佳膳食碳水化合物量和类型得出确凿结论之前,还需要进一步开展研究。