Hans Peter Dr. Krause

Inhibition of Disaccharide Digestion in Rat Intestine by the α-Glucosidase Inhibitor Acarbose (BAY g 5421)

Administration of the alpha-glucosidase inhibitor, acarbose (BAY g 5421), to rats together with a sucrose load results in a marked retardation of sucrose digestion. The carbohydrate content of the small intestine is dose dependently increased; the time needed for the absorption is doubled. In the large intestine significant amounts of carbohydrate can be found only after administration of high doses of acarbose (2-4 mg/kg p.o.). In oral sucrose and maltose loading tests the blood glucose increase is dose dependently reduced by acarbose (ED50, 1 or 12 mg/kg, respectively). In perfused jejunal loops of rats, acarbose inhibits the absorption of sucrose (4 g/l) and maltose (1 and 2 g/l), the IC50 values being 3.2, 36, and 57 micrograms/ml, respectively. The data indicate that acarbose effectively inhibits sucrose digestion. It is 10-20 times less effective with maltose as a substrate. Slight malabsorption is induced by acarbose only in doses higher than the ED50.

Pharmacological Characterization of Bay G 5421, A Glucosidase Inhibitor for the Treatment of Carbohydrate-Dependent Metabolic Disorders

BAY g 5421* delays starch as well as sucrose digestion in the small intestine by inhibiting glucosidases involved in the hydrolysis of oligosaccharides. As a consequence in loading tests with both carbohydrates the blood glucose and serum insulin increments are reduced in animals and in man. The ED 50 is approximately 0.5–3 mg BAY g 5421/kg per os.