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Smoking, inflammatory patterns and postprandial hypertriglyceridemia.

Edmond K Kabagambe¹, Jose M Ordovas, Michael Y Tsai

¹Department of Epidemiology, University of Alabama at Birmingham, 35294, United States. edmondk@uab.edu

Atherosclerosis

|September 23, 2008

Summary

Smoking significantly increases postprandial hypertriglyceridemia (PPT) in fat metabolism. However, inflammation and insulin resistance do not fully explain this effect in smokers.

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Area of Science:

Cardiovascular Health
Metabolic Syndrome
Lipid Metabolism

Background:

Smoking is a known risk factor for elevated triglycerides after meals (postprandial hypertriglyceridemia).
Inflammation and insulin resistance are hypothesized to mediate the link between smoking and postprandial hypertriglyceridemia.

Purpose of the Study:

To investigate whether inflammatory patterns or insulin resistance explain the association between smoking and postprandial hypertriglyceridemia (PPT).

Main Methods:

The study analyzed data from 1036 participants in the NHLBI Genetics of Lipid-Lowering Drugs and Diet Network (GOLDN) study.
Participants consumed a high-fat milkshake, and triglyceride levels were measured over 6 hours.
Inflammatory markers and insulin resistance (HOMA-IR) were assessed, and principal component analysis identified inflammatory patterns.

Main Results:

Current smokers exhibited significantly higher triglyceride levels post-meal compared to never and past smokers.
Two distinct inflammatory patterns were identified: CRP-IL6 and MCP1-TNF-alpha.
The association between smoking and PPT remained significant even after adjusting for insulin resistance and inflammatory patterns.

Conclusions:

The findings confirm that smoking impairs fat metabolism, leading to increased postprandial hypertriglyceridemia.
Mechanisms beyond inflammation and insulin resistance likely contribute to the observed hypertriglyceridemia in smokers.