title: Smoking, inflammatory patterns and postprandial hypertriglyceridemia.
abstract: BACKGROUND
  Smoking is associated with increased postprandial hypertriglyceridemia (PPT). Inflammation and insulin resistance are potential "drivers" for this phenomenon. We tested whether inflammatory patterns and/or insulin resistance explain the effect of smoking on PPT.
  
  
  RESULTS
  Men and women in the NHLBI Genetics of Lipid-Lowering Drugs and Diet Network (GOLDN) study (n=1036, age 49+/-16y) were included. Each participant was asked to suspend use of lipid-lowering drugs for 3 weeks and was given a high-fat milkshake (83% fat and 700kcal/m(2)). Triglyceride concentrations at 0, 3.5 and 6h after the fat load were measured. Inflammatory markers were measured at baseline. Principal component analysis was used to derive inflammatory patterns from individual inflammatory markers (hsCRP, IL2 soluble receptor-alpha, IL6, TNF-alpha and MCP1). Insulin resistance (IR) was estimated using the HOMA equation. Repeated measures-ANOVA was used for analyses. Two inflammatory patterns, namely CRP-IL6 pattern and MCP1-TNF-alpha pattern, were derived. We found significant main (smoking and time) and interaction (smokingxtime) effects (P<0.01) for triglycerides. The multivariate-adjusted triglyceride (mg/dL) concentrations (mean+/-S.E.M.) for never, past and current smokers were 127.38+/-1.04, 119.82+/-1.05 and 134.92+/-1.08 at 0h; 229.42+/-1.04, 238.39+/-1.05 and 293.94+/-1.08 at 3.5h; and 194.63+/-1.04, 208.38+/-1.05 and 248.27+/-1.08 at 6h after the fat load, respectively. Smoking remained significant after adjusting for HOMA-IR and/or inflammatory patterns which showed independent associations with PPT (P<0.05).
  
  
  CONCLUSIONS
  These data confirm impaired metabolism of fat among smokers and suggest that mechanisms other than inflammation or insulin resistance may explain the observed hypertriglyceridemia among smokers.
authors.affiliation: Department of Epidemiology, University of Alabama at Birmingham, 35294, United States. edmondk@uab.edu
authors.forename: Edmond K
authors.initials: EK
authors.lastname: Kabagambe
authors.forename: Jose M
authors.initials: JM
authors.lastname: Ordovas
authors.forename: Michael Y
authors.initials: MY
authors.lastname: Tsai
authors.forename: Ingrid B
authors.initials: IB
authors.lastname: Borecki
authors.forename: Paul N
authors.initials: PN
authors.lastname: Hopkins
authors.forename: Stephen P
authors.initials: SP
authors.lastname: Glasser
authors.forename: Donna K
authors.initials: DK
authors.lastname: Arnett
mesh_terms: D000328:Adult; D000368:Aged; D004041:Dietary Fats; D005260:Female; D006801:Humans; D015228:Hypertriglyceridemia / Q000276:immunology* / Q000378:metabolism*; D007249:Inflammation / Q000382:microbiology*; D007333:Insulin Resistance; D008024:Ligands; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress; D047492:Peroxisome Proliferator-Activated Receptors / Q000378:metabolism; D010641:Phenotype; D019518:Postprandial Period; D012907:Smoking; D014280:Triglycerides / Q000378:metabolism
chemical_list: D004041:Dietary Fats; D008024:Ligands; D047492:Peroxisome Proliferator-Activated Receptors; D014280:Triglycerides