Dietary advanced glycation endproducts and oxidative stress: In vivo effects on endothelial function and adipokines

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%*‡ vs. +0%) and leptin (-22%*‡ vs. -13%*), and a significant increase occurred in vascular cell adhesion molecule 1 (+19%*‡ vs. -5%) and thiobarbituric acid reactive substances (+23%*‡ 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%‡ vs. -5%) and E-selectin (+54%*‡ vs. -3%) occurred. Urinary AGEs increased only after HAGE (+51%*‡ vs. -2%; values presented as HAGE vs. LAGE; *P < 0.05 vs. baseline, ‡P < 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.