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Published on: October 12, 2017
Apolipoprotein L-I is positively associated with hyperglycemia and plasma triglycerides in CAD patients with low HDL
Timothy S E Albert1, Philippe N Duchateau, Samir S Deeb
1Department of Medicine, University of Washington, Seattle, WA, USA.
Insights
Plasma triglycerides and hyperglycemia significantly predict apolipoprotein L-I (apoL-I) levels in coronary artery disease patients. Antioxidant vitamins increased apoL-I, while statin therapy did not affect it.
Area of Science:
- Biochemistry
- Cardiovascular Disease Research
- Lipid Metabolism
Background:
- Apolipoprotein L-I (apoL-I) is associated with high-density lipoprotein (HDL) particles and plasma triglycerides (TGs).
- Understanding apoL-I determinants is crucial in dyslipidemic populations, particularly those with coronary artery disease (CAD).
Purpose of the Study:
- To identify biological determinants of plasma apoL-I levels in patients with coronary artery disease and low HDL.
- To investigate the impact of hyperglycemia and lipid parameters on apoL-I levels.
Main Methods:
- Plasma apoL-I levels were measured in 136 CAD subjects enrolled in a prevention trial.
- Multivariate analysis was used to identify predictors of apoL-I, including VLDL-TG and hyperglycemia (HG).
- The effect of simvastatin-niacin therapy and antioxidant vitamins on apoL-I levels was assessed.
Main Results:
- Plasma apoL-I levels were positively correlated with VLDL-TG and hyperglycemia (HG).
- Hyperglycemic patients exhibited over 50% higher mean apoL-I levels compared to normoglycemic subjects.
- Antioxidant vitamins significantly increased apoL-I levels, whereas simvastatin-niacin therapy did not.
Conclusions:
- Triglycerides (TG) and hyperglycemia (HG) are the primary predictors of apoL-I in dyslipidemic CAD patients.
- These findings contribute to characterizing the novel HDL-associated apoL-I and its relationship with metabolic factors.
Abstract:
Apolipoprotein L-I (apoL-I) is present on a subset of HDL particles and is positively correlated with plasma triglycerides (TGs). We measured plasma apoL-I levels in coronary artery disease (CAD) subjects with low HDL who were enrolled in an angiographic CAD prevention trial. At baseline, apoL-I levels (n = 136; range, 2.2-64.1 mug/ml) were right skewed with a large degree of variability. Multivariate analysis for biological determinants of apoL-I revealed that the log of VLDL-TG (+0.17; P < 0.05) and hyperglycemia (HG; +0.26; P < 0.005) independently predicted apoL-I level. Hyperglycemic patients (n = 24) had mean apoL-I levels >50% higher than normoglycemic subjects (n = 112; 13.2 vs. 8.3 mug/ml, respectively; P < 0.001). No relationship between apoL-I level and change in CAD was found (r = 0.06, P = 0.49). Simvastatin-niacin therapy did not alter apoL-I levels (n = 34; P = 0.27), whereas antioxidant vitamins alone increased apoL-I by >50% (n = 36; P < 0.01). Genotyping of a known apoL-I polymorphism (Lys166Glu) did not independently account for any of the variability in apoL-I levels. In conclusion, we found TG and HG to be the strongest predictors of apoL-I within a dyslipidemic CAD population. These data provide further characterization of the novel HDL-associated apoL-I.
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