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Current smokers with hyperlipidemia lack elevated preβ1-high-density lipoprotein concentrations
Yuki Nagao1, Satoshi Hirayama1, Mika Kon1
1Department of Clinical Laboratory Medicine, Graduate School of Medicine, Juntendo University, Bunkyo-ku, Tokyo, Japan.
Journal of Clinical Lipidology
|April 11, 2017
Summary
Smoking alters prebeta1-high-density lipoprotein (HDL) metabolism, particularly in individuals with hyperlipidemia. This suggests smoking may negatively impact cardiovascular health by affecting cholesterol transport.
Area of Science:
- Cardiovascular Science
- Lipid Metabolism
- Atherosclerosis Research
Background:
- Prebeta1-high-density lipoprotein (HDL) efficiently accepts cell-derived free cholesterol.
- Lecithin-cholesterol acyltransferase converts free cholesterol into lipid-rich HDL.
- Elevated prebeta1-HDL is observed in hyperlipidemia, a risk factor for atherosclerosis.
Purpose of the Study:
- To investigate the impact of smoking on prebeta1-HDL concentrations.
- To assess alterations in prebeta1-HDL metabolism due to smoking.
Main Methods:
- Measured prebeta1-HDL concentration and lecithin-cholesterol acyltransferase-dependent conversion rate (CHTpreβ1) in 74 men (39 nonsmokers, 35 smokers) via immunoassay.
- Grouped participants into normolipidemic and hyperlipidemic categories.
Main Results:
- Nonsmokers: Hyperlipidemic individuals showed 27% higher prebeta1-HDL than normolipidemic individuals (P < .01).
- Smokers: No significant difference in prebeta1-HDL between hyperlipidemic and normolipidemic smokers.
- Correlation: Positive correlation between prebeta1-HDL and CHTpreβ1 in nonsmokers, absent in smokers.
Conclusions:
- Smoking appears to disadvantage individuals with hyperlipidemia by altering prebeta1-HDL metabolism.
- Prebeta1-HDL concentrations were lower in hyperlipidemic smokers compared to nonsmokers.
- CHTpreβ1 was not a significant determinant of prebeta1-HDL in smokers.