title: Postprandial monocyte activation in response to meals with high and low glycemic loads in overweight women.
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 that this is mediated by elevated circulating triacylglycerol-rich lipoproteins.
  
  
  METHODS
  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.affiliation: Division of Endocrinology, Clinical Nutrition, and Vascular Medicine, Department of Internal Medicine, University of California, Davis, CA 95616, USA.
authors.forename: Deborah D
authors.initials: DD
authors.lastname: Motton
authors.forename: Nancy L
authors.initials: NL
authors.lastname: Keim
authors.forename: Fatima A
authors.initials: FA
authors.lastname: Tenorio
authors.forename: William F
authors.initials: WF
authors.lastname: Horn
authors.forename: John C
authors.initials: JC
authors.lastname: Rutledge
mesh_terms: D000328:Adult; D019540:Area Under Curve; D050197:Atherosclerosis / Q000097:blood / Q000453:epidemiology / Q000209:etiology; D001786:Blood Glucose / Q000378:metabolism; D018592:Cross-Over Studies; D016207:Cytokines / Q000096:biosynthesis; D004040:Dietary Carbohydrates / Q000378:metabolism*; D005260:Female; D005434:Flow Cytometry; D038321:Glycemic Index; D006801:Humans; D007328:Insulin / Q000378:metabolism; D053583:Interleukin-1beta / Q000378:metabolism; D008875:Middle Aged; D009000:Monocytes / Q000378:metabolism*; D009765:Obesity / Q000276:immunology* / Q000378:metabolism; D019518:Postprandial Period; D014280:Triglycerides / Q000097:blood*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*
chemical_list: D001786:Blood Glucose; D016207:Cytokines; D004040:Dietary Carbohydrates; D007328:Insulin; D053583:Interleukin-1beta; D014280:Triglycerides; D014409:Tumor Necrosis Factor-alpha