Study on risk reduction of lifestyle-related diseases due to modulations of digestion/absorption capability of carbohydrates.

在动物模型和人类受试者中检验了由于碳水化合物消化/吸收迟缓而抑制餐后高血糖导致慢性炎症和由此产生的生活方式相关疾病风险降低的假设。给2型糖尿病模型大鼠喂食含有抗性淀粉（RS）或α -葡萄糖苷酶抑制剂（米格列醇）的饮食，可降低餐后血糖水平，抑制脂肪组织和外周白细胞中炎症相关基因的表达，同时降低主动脉组织中细胞粘附分子的表达。进食抗氧化食物因子如EGCG可抑制餐后高血糖相关炎症。对健康受试者的横断面研究表明，较高的进食率与血浆IL-1b水平相关，这表明IL-1b是炎症的标志，可能是由高血糖引起的。

The hypothesis that suppression of postprandial hyperglycemia due to retardation of digestion/absorption of carbohydrates leads to reductions of chronic inflammation and resulting lifestyle-related disease risk, was examined in animal models and human subjects.Feeding a diet containing resistant starch (RS) or alpha-glucosidase inhibitor (miglitol) in type 2 diabetes model rats caused a reduction in postprandial glycemic levels, and it led to suppression of inflammation-related gene expressions in adipose tissue and peripheral leukocytes, along with reduced expression of cell adhesion molecules in aorta tissue. The postprandial hyperglycemia-associated inflammation was suppressed by consumption of anti-oxidation food factors such as EGCG. Cross-sectional studies of healthy subjects showed that a higher rate of eating is associated with plasma IL-1b levels, suggesting that IL-1b is a marker for inflammation, presumably caused by hyperglycemia.