Department of Human Nutrition, University of Copenhagen, Frederiksberg C, Denmark.
Am J Clin Nutr. 2011 Aug;94(2):472-8. doi: 10.3945/ajcn.111.014225. Epub 2011 Jun 15.
On the basis of results in cell cultures, rodents, and pigs, l-arabinose may inhibit intestinal sucrase activity and thereby delay sucrose digestion.
The objective was to investigate the dose-response effects of l-arabinose on intestinal sucrase activity in vitro and glucose tolerance, appetite, and energy intake in humans.
In vitro, Caco-2 cells were cultured for 21 d, homogenized, and used as an enzyme preparation with sucrose as substrate in concentrations from 7 to 280 mmol/L with 0.84, 1.4, and 2.8 mmol l-arabinose/L as inhibitor. Released glucose was measured after 30 min. In the human studies, 15 healthy men participated in a randomized, double-blind, crossover study. Sucrose beverages (75 g in 300 mL) supplemented with 0%, 1.3%, 2.7%, and 4% by weight of l-arabinose were tested at breakfast. Blood for the measurement of glucose, insulin, C-peptide, incretin hormones, and triacylglycerol was collected under fasting conditions and for 3 h postprandially. Postprandial appetite sensations and energy intake at lunch were registered.
In vitro, the addition of l-arabinose resulted in uncompetitive inhibition of sucrase activity. In the human studies, supplementation with 4% l-arabinose produced an 11% lower glucose peak, a 33% lower and delayed insulin peak, a 23% reduction in the incremental area under the curve (iAUC) for insulin, a 23% lower and delayed C-peptide peak, a 9% reduction in the iAUC for C-peptide, a 53% increase in the iAUC for glucagon-like peptide-1 (GLP-1), and a 28% reduction in the iAUC for glucose-dependent insulinotropic polypeptide. No effects on triacylglycerol, gastrointestinal symptoms, appetite ratings, or energy intake were observed.
l-Arabinose inhibits sucrase activity from Caco-2 cells; 4% l-arabinose in sucrose beverages reduces postprandial glucose, insulin, and C-peptide responses and enhances the GLP-1 response in humans without gastrointestinal adverse effects. This trial is registered at clinicaltrials.gov as NCT00302302.
基于细胞培养、啮齿动物和猪的研究结果，L-阿拉伯糖可能会抑制肠道蔗糖酶的活性，从而延缓蔗糖的消化。
本研究旨在调查 L-阿拉伯糖对体外肠道蔗糖酶活性以及人体葡萄糖耐量、食欲和能量摄入的剂量反应。
在体外，将 Caco-2 细胞培养 21 天，匀浆后，用蔗糖作为底物，浓度范围为 7 至 280mmol/L，分别添加 0.84、1.4 和 2.8mmol/L 的 L-阿拉伯糖作为抑制剂。30 分钟后测量释放的葡萄糖。在人体研究中，15 名健康男性参与了一项随机、双盲、交叉研究。早餐时，用 0%、1.3%、2.7%和 4%（按重量计）的 L-阿拉伯糖补充的蔗糖饮料（300ml 中含 75g 蔗糖）进行测试。在空腹和餐后 3 小时采集血液以测量血糖、胰岛素、C 肽、肠促胰岛素激素和三酰甘油。记录餐后食欲和午餐时的能量摄入。
体外研究表明，L-阿拉伯糖的添加导致蔗糖酶活性的竞争性抑制。在人体研究中，4%的 L-阿拉伯糖补充剂使葡萄糖峰值降低 11%，胰岛素峰值降低 33%且延迟，胰岛素增量 AUC 降低 23%，C 肽峰值降低 23%，C 肽增量 AUC 降低 9%，胰高血糖素样肽-1（GLP-1）增量 AUC 增加 53%，葡萄糖依赖性胰岛素释放肽（GIP）增量 AUC 降低 28%。未观察到三酰甘油、胃肠道症状、食欲评分或能量摄入的变化。
L-阿拉伯糖抑制 Caco-2 细胞的蔗糖酶活性；蔗糖饮料中 4%的 L-阿拉伯糖可降低人体餐后血糖、胰岛素和 C 肽反应，并增强 GLP-1 反应，而无胃肠道不良反应。该试验在 clinicaltrials.gov 注册，编号为 NCT00302302。
