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

Alaa Alkhalaf*, Nanne Kleefstra, Klaas H. Groenier, Henk J. G. Bilo, Reinold O. B. Gans, Peter Heeringa, Jean L. Scheijen, Casper G. Schalkwijk, Gerjan J. Navis, Stephan J. L. Bakker

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

28 Citations (Web of Science)

Abstract

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
Pages (from-to)e40427
JournalPLOS ONE
Volume7
Issue number7
DOIs
Publication statusPublished - 6 Jul 2012

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