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.
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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.
Authors: Marijke A de Vries; Arash Alipour; Erwin Birnie; Andrew Westzaan; Selvetta van Santen; Ellen van der Zwan; Anho H Liem; Noëlle van der Meulen; Manuel Castro Cabezas Journal: Front Med Date: 2016-02-01 Impact factor: 4.592