|Motton, Deborah - UC-DAVIS JUNIOR FACULTY|
|Tenorio, Fatima - UC-DAVIS STAFF|
|Rutledge, John - UC-DAVIS FACULTY|
Submitted to: American Journal of Clinical Nutrition
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: January 1, 2007
Publication Date: January 11, 2007
Repository URL: http://www.ajcn.org/cgi/reprint/85/1/60
Citation: Keim, N.L., Motton, D.D., Tenorio, F.A., Horn, W.F., Rutledge, J.C. 2007. POSTPRANDIAL MONOCYTE ACTIVATION IN RESPONSE TO MEALS WITH HIGH AND LOW GLYCEMIC LOADS IN OVERWEIGHT WOMEN. American Journal of Clinical Nutrition. 85:60-65, 2007. Interpretive Summary: Several large survey studies have shown that a high carbohydrate diet with high glycemic index is associated with increased risk of heart disease, but the scientific explanation of this association is not known. We conducted a controlled feeding trial in overweight women to determine if the consumption of a high-carbohydrate meal with a high glycemic index led to increases in several factors known to be involved in the inflammation and infiltration of blood vessels – these factors are known to contribute to the development of plaque formation in major blood vessels and subsequent heart disease. We found that some of these factors were elevated following the high glycemic index meal and also following the control meal that had a low glycemic index. In response to both meals, one factor remained elevated for 8 hours after meal ingestion. This prolonged inflammatory response was equivalent to or greater than that observed following ingestion of a high fat meal. These findings suggest that following consumption of meals with high carbohydrate content, there are increases in inflammatory factors that affect the formation of plaque in blood vessels. However, this inflammatory response was not affected by the glycemic index of the meals.
Technical Abstract: Background: Recent data show that atherosclerosis is initiated and perpetuated by inflammatory events. Activation of immune cells such as monocytes initiates inflammation, a key step in atherosclerosis. Objective: We hypothesize that a high glycemic load meal activates inflammatory cells, and this is mediated by increased circulating triacylglycerol-rich lipoproteins. Design: 16 females (BMI 25.7-29.6), aged 20-48 years, consumed meals with a high and low glycemic load in a crossover fashion. Blood samples were collected before and up to 8 h after the meals. Samples were analyzed for glucose, insulin, triacylglycerols, circulating cytokines, and expression of tumor necrosis factor-alpha (TNF-a) and interleukin-1 beta (IL-1b) using flow cytometry. Results: At 3.5 h and 8 h following the test meals, we observed a significant increase in monocytes expressing TNF-a with both high and low glycemic load meals. Also, expression of IL-b' in monocytes tended to increase, but the change was not significant. The glycemic load of the meal did not influence circulating cytokines and had only minimal effect on postprandial triacylglycerols despite marked postprandial changes in glycemia and circulating insulin concentrations. Conclusions: In the postprandial state, monocytes can be activated by both high and low glycemic load meals. The glycemic load of a single meal did not have an effect on the degree of activation of the monocytes in women who displayed only a modest increase in circulating triacylglycerols in response to test meals. Future studies should examine the effect of glycemic load in subjects who have hyperlipemic response to dietary carbohydrate.