TY - JOUR
T1 - Effect of Benfotiamine on Advanced Glycation Endproducts and Markers of Endothelial Dysfunction and Inflammation in Diabetic Nephropathy
AU - Alkhalaf, Alaa
AU - Kleefstra, Nanne
AU - Groenier, Klaas H.
AU - Bilo, Henk J. G.
AU - Gans, Reinold O. B.
AU - Heeringa, Peter
AU - Scheijen, Jean L.
AU - Schalkwijk, Casper G.
AU - Navis, Gerjan J.
AU - Bakker, Stephan J. L.
PY - 2012/7/6
Y1 - 2012/7/6
N2 - 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.
AB - 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.
U2 - 10.1371/journal.pone.0040427
DO - 10.1371/journal.pone.0040427
M3 - Article
C2 - 22792314
SN - 1932-6203
VL - 7
SP - e40427
JO - PLOS ONE
JF - PLOS ONE
IS - 7
ER -