Aim/hypothesis:Short-lasting hyperglycemia results in activation of the transcription factor NF-kB in peripheral blood mononuclearcells. We therefore studied whether the postprandial increase in glucose is sufficient to induce mononuclear NF-kB activation and whether bluntiong postprandial hyperglycemia with the alpha-glucosidase inhibitor acarbose reduces NF-kB activation.
Methods:20 patients with type 2 diabetes were included in a double-blind randomized trial receiving 100 mg acarbose or placebo three times a day over a period of eight weeks. Peripheral blood mononuclear cells were isolated before and 120 minutes after a standardized breakfast. NF-kB binding activity was estimated by electrophoretic mobility shift assay and NF-kB-p65; translocation was determined by Western blot.
Results: Eight weeks of treatment with acarbose significantly reduced postprandial hyperglycemia(p=0.004 when compared to placebo), postprandial mononuclear NF-kB-binding activeity(p=0.045) and nuclear translocation of NF-kB-p65(p=0.02).
Conclusion:Reduction of postprandial glucose peak levels by acarbose reduces postprandial mononuclear NF-kB activation. |