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Postprandial hyperglycaemia and alpha-glucosidase inhibitors.

Diabetes research and clinical practice (1998-09-18)
A D Baron
ABSTRACT

Fasting blood glucose level is usually used to diagnose diabetes, but is not a good predictor of postprandial hyperglycaemia, which is a more accurate measure of the metabolic defect underlying type 2 diabetes. Postprandial blood glucose levels may be elevated while fasting levels are normal, constituting an early stage in type 2 diabetes that can be termed 'postprandial diabetes'. Prevention of postprandial hyperglycaemia is important, as it is implicated in the development of macro- and microvascular complications associated with diabetes. The risk of cardiovascular disease is higher in individuals with postprandial hyperglycaemia, even without diabetes, than in individuals with normal postprandial blood glucose levels. Furthermore, postprandial hyperglycaemia is implicated in the development of type 2 diabetes. Even modest postprandial hyperglycaemia may lead to beta-cell dysfunction. Agents that reduce postprandial hyperglycaemia have a key role in the treatment of type 2 diabetes and pre-diabetic states. Most anti-diabetic agents that are currently available reduce fasting blood glucose levels, but have little impact on postprandial glycaemic excursions and thus do not normalize postprandial hyperglycaemia. However, new agents that control postprandial hyperglycaemia have been developed, for example, the alpha-glucosidase inhibitor acarbose. Such agents have a potential to reduce the progression of diabetes as well as macro- and microvascular complications.

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Sigma-Aldrich
α-Glucosidase from Saccharomyces cerevisiae, Type I, lyophilized powder, ≥10 units/mg protein (using p-nitrophenyl α-D-glucoside as substrate.)
Sigma-Aldrich
α-Glucosidase from Bacillus stearothermophilus, lyophilized powder, ≥50 units/mg protein