Reduction of Postprandial Hyperglycemia in Patients with Type 2 Diabetes Reduces NF-κB Activation in PBMCs

Abstract

Aims/hypothesis: Short-lasting hyperglycemia results in activation of the transcription factor NF-κB in peripheral blood mononuclear cells. We therefore studied whether the postprandial increase in glucose is sufficient to induce mononuclear NF-κB activation and whether blunting postprandial hyperglycemia with the alpha-glucosidase inhibitor acarbose reduces NF-κB 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-κB binding activity was estimated by electrophoretic mobility shift assay and NF-κB-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-κB-binding activity (p = 0.045) and nuclear translocation of NF-κB-p65 (p = 0.02).

Conclusion: Reduction of postprandial glucose peak levels by acarbose reduces postprandial mononuclear NF-κB activation.

Key words

Postprandial hyperglycemia · Activation of NF-kappa B · Acarbose · Peripheral mononuclear cells · Type 2 diabetes

References

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