Hypertriglyceridaemia among smokers may be accounted for by mechanisms other than inflammation and insulin resistance
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Smoking appears to be associated with increased postprandial hypertriglyceridaemia (PPT), which may be accounted for by inflammation and insulin resistance as potential “drivers”. This study was conducted to test whether inflammatory patterns and/or insulin resistance explain the effect of smoking on PTT. A total of 1036 men and women participating in the NHLBI Genetics of Lipid-Lowering Drugs and Diet Network (GOLDN) study were included, with each participant being asked to suspend use of lipid-lowering drugs for 3 weeks and being given a high-fat milkshake. Insulin resistance was estimated using HOMA-IR equation. Two inflammatory patterns, namely CRP-IL6 pattern and MCP1-TNF-alpha pattern, were derived from individual inflammatory markers. Significant main (smoking and time) and interaction (smoking x time) effects were observed for triglycerides. After adjusting for HOMA-IR and/or inflammatory patterns, smoking remained significantly and independently associated with PPT. These results confirm the presence of impaired triglyceride metabolism among smokers, independent of factors known to affect lipid levels (e.g. alcohol, gender, diet, hypertension, and physical activity), thus suggesting that hypertriglyceridaemia among smokers might be accounted for by mechanisms other than inflammation or insulin resistance.
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