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 that this is mediated by elevated circulating triacylglycerol-rich lipoproteins.
Design: Sixteen women [body mass index (in kg/m2): 25.7-29.6], aged 20-48 y, consumed meals with a high or a low glycemic load in a crossover fashion. Blood samples were collected before and up to 8 h after the meals. Samples were measured for glucose, insulin, triacylglycerols, and circulating cytokines, and expression of tumor necrosis factor alpha (TNF-alpha) and interleukin 1beta (IL-1beta) was measured by flow cytometry.
Results: At 3.5 h after the test meals, we observed a significant increase in monocytes expressing TNF-alpha with both high-and low-glycemic load meals. Also, expression of IL-1beta 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 a minimal effect on postprandial triacylglycerol concentrations 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 a significant 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 a hyperlipemic response to dietary carbohydrate.