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Pharmacology of α‐glucosidase inhibition
Author(s) -
AG H. BISCHOFF Bayer
Publication year - 1994
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1111/j.1365-2362.1994.tb02249.x
Subject(s) - acarbose , postprandial , glycation , endocrinology , diabetic nephropathy , diabetes mellitus , medicine , pharmacology , blood sugar , disaccharidase , brush border , dipeptidyl peptidase 4 , sucrase , chemistry , biochemistry , enzyme , small intestine , type 2 diabetes , vesicle , membrane
The development of α‐amylase and brush‐border α‐glucosidase inhibitors is reviewed. The mode of action as well as pharmacological and pharmacodynamic properties of selected inhibitors with special regard to the most thoroughly investigated α‐glucosidase inhibitor acarbose are discussed. Inhibition of intestinal α‐glucosidases delays the digestion of starch and sucrose, flattens the postprandial blood glucose excursions, and thus mimics the effects of dieting on hyperglycaemia, hyperinsulinaemia and hypertriglyceridaemia. Therefore, the mechanism of α‐glucosidase inhibition represents the pharmacological optimization of the dietary principle of delayed carbohydrate absorption. In pre‐clinical studies using diabetic animals the oral administration of acarbose improved the metabolic state and reduced the blood glucose area under the curve. As a consequence, the process of non‐enzymatic glycation of proteins was retarded as indicated by reduced glycated haemoglobin, glomerular basement membranes or advanced glycation end‐products (AGEs) in collagen. These improved biochemical parameters correlated with beneficial effects against the development of diabetic nephropathy and neuropathy. Thus, the treatment of diabetic animals with acarbose does not only improve the metabolic state but has also the potential to delay, or possibly prevent, the development of diabetic complications.