INFLUENCE OF ACARBOSE ON POSTPRANDIAL DYSMETABOLISM: RESULTS OF AN OPEN-LABEL RANDOMIZED STUDY

Abstract

Aim: To evaluate postprandial changes of lipid and glucose profiles, inflammation markers levels and flow-mediated vasodilatation in patients with metabolic syndrome (MS) and to estimate acarbose course treatment efficacy in glucose intolerant patients. Material and methods: A total of 114 MS patients (83 men, 31 women) were examined, MS was associated with impaired glucose tolerance (IGT) in 55 cases. At the first stage postprandial dynamics of flow-mediated dilation (FMD), lipid profile parameters, inflammation markers and insulin levels were estimated. At the second stage patients with MS and IGT (n=55) were randomly assigned to the two groups of treatment. Patients of the first group (n=28) had non-drug treatment. Patients of the second group (n=27) received acarbose 300 mg/day for 3 months in addition to recommendations for lifestyle change. 3 months later postprandial values of lipid and glucose profiles parameters, inflammation markers levels and FMD were reassessed. Results: MS patients with IGT revealed maximal disorders in metabolic parameters during postprandial period: increase in the plasma levels of total cholesterol by 6.1%, high density lipoproteins-by 1.7%, and triglycerides-by 27.87%, increase in atherogenic index by 4.8%, and plasma concentrations of glucose-by 54.7%, insulin-by 30.2%, HOMA index-by 73.3%, as well as concentrations of C-reactive protein (CRP)-by 49.7%, tumor necrose factor alpha-by 20.8%, and interleukin-6 (IL-6)-by 51.9%. FMD decreased by 34.3%. After 12 weeks of the acarbose treatment we had revealed positive dynamics of studied indices in postprandial period as compared to an only non-drug management: levels of glucose increased by 24.1% vs 44.4%, insulin-by 14.4% vs 24.4%, CRP-by 19.9% vs 36.6%, IL-6-by 25.1% vs 41.7%; postprandial FMD decreased by 18.9% vs 31.1%. Conclusion: Prescription of acarbose 300 mg/day for 12 weeks in glucose intolerant patients is characterized by less significant postprandial increase in insulin resistance, inflammation markers (CRP and IL-6) levels, less decrease in flow-mediated vasodilatation with no influence on lipid metabolism parameters.