Postprandial monocyte activation in response to meals with high and low glycemic loads in overweight women  

Oleh:

Motton, Deborah D. ; Keim, Nancy L ; Tenorio, Fatima A. ; Horn, William F. ; Rutledge, John C.

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: The American Journal of Clinical Nutrition vol. 85 no. 01 (Jan. 2007), page 60.
Topik: Monocytes • inflammation • tumor necrosis factor • interleukin 6 • glycemic index • insulin • glucose • triacylglycerols • obesity • carbohydrates

Ketersediaan

Perpustakaan FK Nomor Panggil: A07.K.2007.01 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Isi artikel

1 From the Division of Endocrinology, Clinical Nutrition, and Vascular Medicine, Department of Internal Medicine, University of California, Davis (DDM, FAT, and JCR), and the Western Human Nutrition Research Center, Agricultural Research Service, US Department of Agriculture, University of California, Davis (NLK and WFH). 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 (TNF-) and interleukin 1ß (IL-1ß) was measured by flow cytometry. Results: At 3.5 h after the test meals, we observed a significant increase in monocytes expressing TNF- with both high–and low–glycemic load meals. Also, expression of IL-1ß 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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