title: Dietary advanced glycation endproducts and oxidative stress: in vivo effects on endothelial function and adipokines.
abstract: Advanced glycation endproducts (AGEs) and oxidative stress (OS) contribute to the development and progression of diabetic complications. We have reported that dietary AGEs and OS induce acute endothelial dysfunction in vivo, but little is known about their effects on adipokines. Twenty inpatients with type 2 diabetes mellitus (mean age: 55.9; range: 32-71 years), received a standard diabetes diet for 6 days. On days 4 and 6, the acute effects of a high-AGE (HAGE) or a low-AGE (LAGE) meal (15.100 vs. 2.750 kU AGE) were studied in a randomized, cross-over, investigator-blinded design. Measurements were performed after an overnight fast, at baseline (B) and at 2, 4, and 6 h after the HAGE or LAGE meals. Both meals had the same ingredients and differed only by the cooking method. Two h following HAGE, a significant decrease from baseline occurred in adiponectin (-10%*double dagger vs. +0%) and leptin (-22%*double dagger vs. -13%*), and a significant increase occurred in vascular cell adhesion molecule 1 (+19%*double dagger vs. -5%) and thiobarbituric acid reactive substances (+23%*double dagger vs. +6%). These changes did not occur, or occurred to a lesser extent, following LAGE. At 4 h following HAGE, an increase in methylglyoxal (+20%double dagger vs. -5%) and E-selectin (+54%*double dagger vs. -3%) occurred. Urinary AGEs increased only after HAGE (+51%*double dagger vs. -2%; values presented as HAGE vs. LAGE; *P < 0.05 vs. baseline, double daggerP < 0.05 vs. LAGE). The postprandial excursions in glucose, insulin, and triglycerides were similar between both meals. A meal rich in AGEs induces acute endothelial and adipocyte dysfunction. These effects were prevented by changing the cooking method.
authors.affiliation: Diabetes Center North Rhine-Westphalia, Bad Oeynhausen, Germany. astirban@hdz-nrw.de
authors.forename: Alin
authors.initials: A
authors.lastname: Stirban
authors.forename: Monica
authors.initials: M
authors.lastname: Negrean
authors.forename: Christian
authors.initials: C
authors.lastname: Götting
authors.forename: Jaime
authors.initials: J
authors.lastname: Uribarri
authors.forename: Thomas
authors.initials: T
authors.lastname: Gawlowski
authors.forename: Bernd
authors.initials: B
authors.lastname: Stratmann
authors.forename: Knut
authors.initials: K
authors.lastname: Kleesiek
authors.forename: Theodor
authors.initials: T
authors.lastname: Koschinsky
authors.forename: Helen
authors.initials: H
authors.lastname: Vlassara
authors.forename: Diethelm
authors.initials: D
authors.lastname: Tschoepe
mesh_terms: D054392:Adipokines / Q000502:physiology*; D052242:Adiponectin / Q000097:blood; D000328:Adult; D017668:Age of Onset; D000368:Aged; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000378:metabolism*; D004032:Diet; D019040:E-Selectin / Q000097:blood; D004730:Endothelium, Vascular / Q000502:physiology*; D005260:Female; D017127:Glycation End Products, Advanced / Q000378:metabolism*; D006801:Humans; D007297:Inpatients; D020738:Leptin / Q000097:blood; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress / Q000502:physiology*; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D014443:Tyrosine / Q000031:analogs & derivatives / Q000097:blood
chemical_list: D054392:Adipokines; D052242:Adiponectin; D019040:E-Selectin; D017127:Glycation End Products, Advanced; D020738:Leptin; D017392:Thiobarbituric Acid Reactive Substances; C002744:3-nitrotyrosine; D014443:Tyrosine