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的消化/吸收延迟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。（米格列醇）在2型糖尿病模型大鼠中引起餐后血糖水平降低，并导致脂肪组织和外周白细胞中炎症相关基因表达的抑制，沿着主动脉组织中细胞粘附分子表达的降低。餐后高血糖相关炎症可通过食用抗氧化食物因子（如表没食子酸酯）来抑制。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是炎症的标志物，可能由高血糖引起。

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.