Battilana P, Ornstein K, Minehira K, Schwarz J M, Acheson K, Schneiter P, Burri J, Jéquier E, Tappy L
Institute of Physiology, School of Medicine, University of Lausanne, Switzerland.
Eur J Clin Nutr. 2001 May;55(5):327-33. doi: 10.1038/sj.ejcn.1601160.
To assess whether beta-glucan (which is fermented in the colon) lowers postprandial glucose concentrations through mechanisms distinct from a delayed carbohydrate absorption and inhibits de novo lipogenesis.
Administration of frequent small meals each hour over 9 h allows a rate of intestinal absorption to be reached which is independent of a delayed absorption. A group of 10 healthy men received either an isoenergetic diet containing 8.9 g/day beta-glucan or without beta-glucan for 3 days. On the third day, the diet was administered as fractioned meals ingested every hour for 9 h.
Laboratory for human metabolic investigations.
Ten healthy male volunteers.
Plasma glucose and insulin concentrations, glucose kinetics, glucose oxidation, de novo lipogenesis.
On the third day, plasma glucose and free fatty acid concentrations, carbohydrate and lipid oxidation, and energy expenditure were identical with beta-glucan and cellulose. Plasma insulin concentrations were, however, 26% lower with beta-glucan during the last 2 h of the 9 h meal ingestion. Glucose rate of appearance at steady state was 12% lower with beta-glucan. This corresponded to a 21% reduction in the systemic appearance rate of exogenous carbohydrate with beta-glucan, while endogenous glucose production was similar with both diets. De novo lipogenesis was similar with and without beta-glucan.
Administration of frequent meals with or without beta-glucan results in similar carbohydrate and lipid metabolism. This suggests that the lowered postprandial glucose concentrations which are observed after ingestion of a single meal containing beta-glucan are essentially due to a delayed and somewhat reduced carbohydrate absorption from the gut and do not result from the effects of fermentation products in the colon.
评估β-葡聚糖(在结肠中发酵)是否通过与碳水化合物吸收延迟不同的机制降低餐后血糖浓度,并抑制从头脂肪生成。
在9小时内每小时频繁给予少量餐食,以使肠道吸收速率达到与吸收延迟无关的水平。一组10名健康男性连续3天接受含8.9克/天β-葡聚糖的等能量饮食或不含β-葡聚糖的饮食。在第三天,饮食以每小时分次进餐的方式给予,持续9小时。
人体代谢研究实验室。
10名健康男性志愿者。
血浆葡萄糖和胰岛素浓度、葡萄糖动力学、葡萄糖氧化、从头脂肪生成。
在第三天,β-葡聚糖组和纤维素组的血浆葡萄糖和游离脂肪酸浓度、碳水化合物和脂质氧化以及能量消耗相同。然而,在9小时进餐的最后2小时内,β-葡聚糖组的血浆胰岛素浓度低26%。β-葡聚糖组稳态时葡萄糖的出现率低12%。这相当于β-葡聚糖组外源性碳水化合物的全身出现率降低21%,而两种饮食的内源性葡萄糖生成相似。有无β-葡聚糖时从头脂肪生成相似。
给予含或不含β-葡聚糖的频繁餐食会导致相似的碳水化合物和脂质代谢。这表明,摄入含β-葡聚糖的单餐后观察到的餐后血糖浓度降低,主要是由于肠道碳水化合物吸收延迟且有所减少,而非结肠发酵产物的作用。