There is a strong role for impaired insulin secretion in the development and progression of type 2 diabetes, in particular due to a deficit in the early phase response to glucose load, as well as increasing insulin resistance (1,2). It is believed that most subjects developing type 2 diabetes pass through a phase of impaired glucose tolerance (IGT). In this process—following the glucose toxicity theory—excessive postprandial hyperglycemia may act in a vicious circle (7), with harmful effects on both the insulin-producing beta-cells (3) and insulin sensitivity (4), leading to chronic hyperglycemia and progressive deterioration of diabetes, as shown in the U.K. Prospective Diabetes Study (UKPDS) (5).
There is increasing evidence that postprandial or 2 h postchallenge hyperglycemia is an independent risk factor for cardiovascular disease (6,7) and all-cause mortality (8-10). Excessive postprandial glucose excursion initiates a cascade of proatherogenic events: increased insulin resistance, activation of low-grade inflammation and blood coagulation as well as oxidative stress. Among other factors (Table 1), postprandial hyperglycemia strongly depends on the amount and of absorbed monosaccharides and velocity of absorption in the small intestine. Carbohydrates should account for ~50% of the daily supply of calories in type 2 diabetes. Monosaccharides play only a minor role as dietary carbohydrates since they consist mainly of complex carbohydrates, such as starch (~60%), and disaccharides, such as sucrose (~30%). Complex carbohydrates and disaccharides must be hydrolyzed by intestinal and pancreatic enzymes before they can be transported through the mucosa of the bowel. Thus, any medication that delays breakdown of complex carbohydrates should decrease postprandial hyperglycemia and improve insulin sensitivity, as well as protecting the beta-cells of the pancreas.
The digestion of complex carbohydrates in the lower parts of the small intestine and upper part of colon, as is the case with natural eating habits, has a stronger stimulating effect on gastrointestinal hormones, such as glucagon-like peptide 1 (GLP1) (12) than consumption of refined carbohydrates as typical for modern fast food. Alpha-glucosidase inhibitors (AGIs— acarbose, miglitol, voglibose) are oral antidiabetics that specifically inhibit a-glucosidases in the brush border of the small intestine. These enzymes are essential for the release of glucose from more complex carbohydrates (14,15).
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