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Isolation and Analysis of Plasma Lipoproteins by Ultracentrifugation
Published on: January 28, 2021
Lipoprotein lipase gene polymorphisms in Croatian patients with coronary artery disease
Goran Ferencak1, Daria Pasalić, Branka Grsković
1Clinical Institute of Laboratory Diagnosis, Clinical Hospital Center and Zagreb University School of Medicine, Zagreb, Croatia. gferen@mef.hr
Insights
Lipoprotein lipase gene variations influence coronary artery disease (CAD) risk and lipid profiles. The N291S polymorphism showed a significant association with CAD, while other variants impacted lipid levels in Croatian patients.
Area of Science:
- Genetics
- Cardiovascular Disease
- Biochemistry
Background:
- Elevated triglycerides and reduced high-density lipoprotein (HDL) are key risk factors for coronary artery disease (CAD).
- Lipoprotein lipase (LPL) plays a crucial role in lipid metabolism, making its gene a potential target for studying CAD predisposition.
- Genetic variations in the LPL gene may influence an individual's susceptibility to CAD and their lipid profiles.
Purpose of the Study:
- To investigate the association between specific LPL gene polymorphisms (-93T/G, D9N, N291S, and S447X) and the risk of CAD.
- To determine the impact of these LPL gene polymorphisms on lipid levels (triglycerides, HDL, HDL2-cholesterol, apolipoprotein A-I) in Croatian patients with and without confirmed CAD.
- To explore potential interactions between LPL gene variants, lipid profiles, and CAD risk.
Main Methods:
- Genotyping of four LPL gene polymorphisms (-93T/G, D9N, N291S, S447X) in Croatian patients.
- Case-control study design comparing patients with and without angiographically confirmed CAD.
- Analysis of lipid profiles, including triglycerides, HDL-cholesterol, HDL2-cholesterol, and apolipoprotein A-I levels.
- Statistical analysis to assess the association between LPL polymorphisms and CAD risk, adjusting for lipid levels.
Main Results:
- The N291S polymorphism was significantly associated with increased CAD risk (OR = 0.36; p = 0.048), an association moderately affected by lipid adjustment.
- Non-carriers of the -93T/G and D9N polymorphisms exhibited significantly higher HDL2-cholesterol and apolipoprotein A-I levels within the CAD group.
- The S447X mutation was linked to lower triglyceride and higher HDL2-cholesterol levels in the control group.
- No significant differences in lipid levels were observed for the N291S variant between carriers and non-carriers.
Conclusions:
- LPL gene polymorphisms, particularly N291S, may play a role in the genetic predisposition to coronary artery disease.
- Specific LPL gene variants are associated with variations in lipid profiles, potentially influencing CAD risk.
- Further research is warranted to elucidate the complex interplay between LPL genetics, lipid metabolism, and cardiovascular disease development.
Abstract:
Modifications in lipoprotein lipase levels lead to elevated triglycerides and reduced high density lipoprotein (HDL), both of which are risk factors for coronary artery disease (CAD). Hence, we examined the influence of the -93T/G, D9N, N291S, and S447X polymorphisms in the lipoprotein lipase (LPL) gene on CAD risk and lipid levels in Croatian patients with and without angiographically confirmed CAD. The N291S polymorphism was significantly associated with CAD (OR = 0.36; 95% CI = 0.13, 0.99; p = 0.048). This association was only moderately affected by adjusting for various lipids (OR = 0.36; 95% CI = 0.12, 1.08; p = 0.068). HDL2-cholesterol and apolipoprotein A-I levels were significantly higher in non-carriers of the -93T/G and D9N polymorphisms in the CAD group (p = 0.017 and 0.028, respectively). The N291S genetic variant did not show any significant difference between carriers and non-carriers in either group studied for any of the lipids. Lower triglyceride and higher HDL2-cholesterol levels in the control group were associated with carriers of the S447X mutation (p = 0.043 and 0.056, respectively). LPL gene polymorphisms might be involved in predisposition to CAD and determination of lipid profiles.
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