Postprandial impairment of flow-mediated dilation and elevated methylglyoxal after simple but not complex carbohydrate consumption in dogs

Hyperglycemia produces oxidative stress, which may impair endothelial function. Methylglyoxal, a reactive intermediate metabolite of glucose, is known to cause oxidative stress and is produced when excess carbohydrate is consumed in diabetic patients, but postprandial responses in healthy patients are unknown. We hypothesize that methylglyoxal levels will cause impaired endothelial function via increased oxidative stress after consuming a high glycemic index meal in healthy animals. Normal-weight laboratory beagles (n = 6) were used in a crossover study that tested postprandial responses of 4 complex carbohydrate sources (barley, corn, peas, rice) vs a simple carbohydrate (glucose). Blood samples were taken prefeeding and at timed intervals after feeding to measure serum glucose, insulin, nitrotyrosine, and methylglyoxal. Flow-mediated dilation (FMD), cardiac function (echocardiography), and blood pressure measurements were determined before and 60 minutes after feeding. The mean (+/- SEM) glycemic indices of the complex carbohydrate sources were 29 +/- 5 for peas, 47 +/- 10 for corn, 51 +/- 7 for barley, and 55 +/- 6 for rice. Postprandial FMD was lowest in the glucose group and significantly different from both the corn group and the FMD value for all complex carbohydrates combined. Methylglyoxal was significantly elevated at 60 minutes postprandial after glucose compared with the other carbohydrate sources. No significant effects of carbohydrate source were observed for blood pressure, nitrotyrosine, or echocardiographic variables. The novel finding of this study was that methylglyoxal levels increased after a single feeding of simple carbohydrate and may be linked to the observed postprandial decrease in endothelial function. Thus, consuming low-glycemic-index foods may protect the cardiovascular system by reducing oxidative stress. (C) 2012 Elsevier Inc. All rights reserved.