Effects of a single administration of acarbose on postprandial glucose excursion and endothelial        dysfunction in type 2 diabetic patients: a randomized cross-over study

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

    This study was aimed to assess the efficacy of acarbose on postprandial metabolic parameters and endothelial function in type 2 diabetic patients. Postprandial peakglucose (14.47 ± 1.27 vs 8.50 ± 0.53 mmol/l), plasma glucose excursion   (PPGE), and ΔAUCglucose 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).

    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 ΔAUC glucose. The peak FBF and   FDR were inversely well correlated with Peakglucose, PPGE and ΔAUCglucose , but not with ΔAUCinsulin nor the other lipid parameters.

    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.