Effect of Benfotiamine on Advanced Glycation Endproducts and Markers of Endothelial Dysfunction and Inflammation in Diabetic Nephropathy

Alkhalaf, A., Kleefstra, N., Groenier, K. H., Bilo, H. J. G., Gans, R. O. B., Heeringa, P., Scheijen, J. L., Schalkwijk, C. G., Navis, G. J. & Bakker, S. J. L., 6-Jul-2012, In : PLoS ONE. 7, 7, 6 p., e40427.

Research output: Contribution to journalArticleAcademicpeer-review

Background: Formation of advanced glycation endproducts (AGEs), endothelial dysfunction, and low-grade inflammation are intermediate pathways of hyperglycemia-induced vascular complications. We investigated the effect of benfotiamine on markers of these pathways in patients with type 2 diabetes and nephropathy.

Methods: Patients with type 2 diabetes and urinary albumin excretion in the high-normal and microalbuminuric range (15-300 mg/24h) were randomized to receive benfotiamine (n = 39) or placebo (n = 43). Plasma and urinary AGEs (N-epsilon-( carboxymethyl) lysine [CML], N-epsilon-(Carboxyethyl) lysine [CEL], and 5- hydro- 5- methylimidazolone [MG- H1]) and plasma markers of endothelial dysfunction (soluble vascular cell adhesion molecule-1 [sVCAM-1], soluble intercellular adhesion molecule- 1 [sICAM-1], soluble E-selectin) and low-grade inflammation (high-sensitivity C-reactive protein [hs-CRP], serum amyloid-A [SAA], myeloperoxidase [MPO]) were measured at baseline and after 6 and 12 weeks.

Results: Compared to placebo, benfotiamine did not result in significant reductions in plasma or urinary AGEs or plasma markers of endothelial dysfunction and low-grade inflammation. Conclusions: Benfotiamine for 12 weeks did not significantly affect intermediate pathways of hyperglycemia-induced vascular complications.

Original languageEnglish
Article numbere40427
Number of pages6
JournalPLoS ONE
Issue number7
Publication statusPublished - 6-Jul-2012



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