Medical Journals

Benfotiamine Prevents Macro- and Microvascular Endothelial Dysfunction and Oxidative Stress Following a Meal Rich in Advanced Glycation End Products in Individuals with Type 2 Diabetes.

Authors:
  • Stirban Alin
  • Negrean Monica
  • Stratmann Bernd
  • Gawlowski Thomas
  • Horstmann Tina
  • Götting Christian
  • Kleesiek Knut
  • Mueller-Roesel Michaela
  • Koschinsky Theodor
  • Uribarri Jaime
  • Vlassara Helen
  • Tschoepe Diethelm

From: Heart and Diabetes Center NRW, Georgstrasse 11, 32545 Bad Oeynhausen, Germany.

Diabetes care

  • Publish Date: Sep 2006
  • ISSN: 0149-5992
  • Volume: 29
  • Issue: 9
  • Pages: 2064-71
  • Medium: Print
  • Language: English
  • Citation (JAMA): Stirban Alin, Negrean Monica, Stratmann Bernd, et al. Benfotiamine Prevents Macro- and Microvascular Endothelial Dysfunction and Oxidative Stress Following a Meal Rich in Advanced Glycation End Products in Individuals with Type 2 Diabetes.. Diabetes Care Sep 2006;29:2064-71

Abstract

OBJECTIVE: Diabetes is characterized by marked postprandial endothelial dysfunction induced by hyperglycemia, hypertriglyceridemia, advanced glycation end products (AGEs), and dicarbonyls (e.g., methylglyoxal [MG]). In vitro hyperglycemia-induced MG formation and endothelial dysfunction could be blocked by benfotiamine, but in vivo effects of benfotiamine on postprandial endothelial dysfunction and MG synthesis have not been investigated in humans until now. RESEARCH DESIGN AND METHODS: Thirteen people with type 2 diabetes were given a heat-processed test meal with a high AGE content (HAGE; 15.100 AGE kU, 580 kcal, 54 g protein, 17 g lipids, and 48 g carbohydrates) before and after a 3-day therapy with benfotiamine (1,050 mg/day). Macrovascular flow-mediated dilatation (FMD) and microvascular reactive hyperemia, along with serum markers of endothelial disfunction (E-selectin, vascular cell adhesion molecule-1, and intracellular adhesion molecule-1), oxidative stress, AGE, and MG were measured during both test meal days after an overnight fast and then at 2, 4, and 6 h postprandially. RESULTS: The HAGE induced a maximum reactive hyperemia decrease of -60.0% after 2 h and a maximum FMD impairment of -35.1% after 4 h, without affecting endothelium-independent vasodilatation. The effects of HAGE on both FMD and reactive hyperemia were completely prevented by benfotiamine. Serum markers of endothelial dysfunction and oxidative stress, as well as AGE, increased after HAGE. These effects were significantly reduced by benfotiamine. CONCLUSIONS: Our study confirms micro- and macrovascular endothelial dysfunction accompanied by increased oxidative stress following a real-life, heat-processed, AGE-rich meal in individuals with type 2 diabetes and suggests benfotiamine as a potential treatment.

Mesh Headings (Keywords): Adjuvants, Immunologic, Biological Markers, Blood Glucose, Cross-Over Studies, Diabetes Mellitus, Type 2, Endothelium, Vascular, Glycosylation End Products, Advanced, Humans, Hyperglycemia, Hypertriglyceridemia, Laser-Doppler Flowmetry, Microcirculation, Middle Aged, Oxidative Stress, Thiamine, Vascular Cell Adhesion Molecule-1, Vascular Diseases


Check for Full Text / PubMed Unique Identifier (PMID): 16936154


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