|Budget Amount *help
¥18,330,000 (Direct Cost: ¥14,100,000、Indirect Cost: ¥4,230,000)
Fiscal Year 2013: ¥5,590,000 (Direct Cost: ¥4,300,000、Indirect Cost: ¥1,290,000)
Fiscal Year 2012: ¥6,370,000 (Direct Cost: ¥4,900,000、Indirect Cost: ¥1,470,000)
Fiscal Year 2011: ¥6,370,000 (Direct Cost: ¥4,900,000、Indirect Cost: ¥1,470,000)
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.