Context: Postprandial hyperglycemia has been reported to elicit endothelial dysfunction and to provoke future cardiovascular complications. A reduction of postprandial blood glucose levels by the -glucosidase inhibitor acarbose was associated with a risk reduction of cardiovascular complications, but effects of acarbose on endothelial function has never been elucidated.

Design: This study was aimed to assess the efficacy of acarbose on postprandial metabolic parameters and endothelial function in type 2 diabetic patients. Postprandial peak_glucose (14.47 ± 1.27 vs. 8.50 ± 0.53 mmol/l), plasma glucose excursion (PPGE), and AUC_glucose after a single loading of test meal (total 450kcal; protein 15.3%; fat 33.3%; carbohydrate 51.4%) were significantly higher in diet-treated type 2 diabetic patients (n = 14) than in age- and sex-matched controls (n = 12).

Results: The peak forearm blood flow (FBF) response and total reactive hyperemic flow (flow debt repayment: FDR) during reactive hyperemia, indices of resistance artery endothelial function on strain-gauge plethysmography, were unchanged before and after meal loading in controls. But those of diabetics were significantly decreased 120 and 240 min after test meal. A prior administration of acarbose decreased postprandial Peak _glucose, PPGE, and AUC_glucose. The peak FBF and FDR were inversely well correlated with Peak_glucose, PPGE and AUC_glucose, but not with AUC_insulin nor the other lipid parameters.

Conclusions: Even a single loading of test meal was shown to impair endothelial function in type 2 diabetic patients, and the postprandial endothelial dysfunction was improved by a prior use of acarbose. Acarbose might reduce macrovascular complication by avoiding endothelial injury in postprandial hyperglycemic status.