Smoking, inflammatory patterns and postprandial hypertriglyceridemia

Edmond K. Kabagambe, Jose M. Ordovas, Michael Y. Tsai, Ingrid B. Borecki, Paul N. Hopkins, Stephen P. Glasser, Donna K. Arnett

Research output: Contribution to journalArticlepeer-review

29 Scopus citations

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. Methods and results: Men and women in the NHLBI Genetics of Lipid-Lowering Drugs and Diet Network (GOLDN) study (n = 1036, age 49 ± 16 y) 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 700 kcal/m2). Triglyceride concentrations at 0, 3.5 and 6 h 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-α, IL6, TNF-α 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-α pattern, were derived. We found significant main (smoking and time) and interaction (smoking × time) 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 0 h; 229.42 ± 1.04, 238.39 ± 1.05 and 293.94 ± 1.08 at 3.5 h; and 194.63 ± 1.04, 208.38 ± 1.05 and 248.27 ± 1.08 at 6 h 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.

Original languageEnglish (US)
Pages (from-to)633-639
Number of pages7
JournalAtherosclerosis
Volume203
Issue number2
DOIs
StatePublished - Apr 2009

Bibliographical note

Funding Information:
Grant/funding support : This study was funded by NHLBI grant number U01HL072524-04.

Keywords

  • Inflammation
  • Insulin resistance
  • Lipids
  • Smoking
  • Triglycerides

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