Apolipoprotein L-I is positively associated with hyperglycemia and plasma triglycerides in CAD patients with low HDL
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 lev...
| Main Authors: | , , , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Elsevier
2005-03-01
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| Series: | Journal of Lipid Research |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S0022227520340311 |
| _version_ | 1818933368956387328 |
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| author | Timothy S.E. Albert Philippe N. Duchateau Samir S. Deeb Clive R. Pullinger Min H. Cho David C. Heilbron Mary J. Malloy John P. Kane B. Greg Brown |
| author_facet | Timothy S.E. Albert Philippe N. Duchateau Samir S. Deeb Clive R. Pullinger Min H. Cho David C. Heilbron Mary J. Malloy John P. Kane B. Greg Brown |
| author_sort | Timothy S.E. Albert |
| collection | DOAJ |
| description | 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 μg/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 μg/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. |
| first_indexed | 2024-12-20T04:47:17Z |
| format | Article |
| id | doaj.art-88120ae0aeab4153a4a082f5167a2b5e |
| institution | Directory Open Access Journal |
| issn | 0022-2275 |
| language | English |
| last_indexed | 2024-12-20T04:47:17Z |
| publishDate | 2005-03-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Journal of Lipid Research |
| spelling | doaj.art-88120ae0aeab4153a4a082f5167a2b5e2022-12-21T19:52:58ZengElsevierJournal of Lipid Research0022-22752005-03-01463469474Apolipoprotein L-I is positively associated with hyperglycemia and plasma triglycerides in CAD patients with low HDLTimothy S.E. Albert0Philippe N. Duchateau1Samir S. Deeb2Clive R. Pullinger3Min H. Cho4David C. Heilbron5Mary J. Malloy6John P. Kane7B. Greg Brown8Department of Medicine, University of Washington, Seattle, WA; Department of Genome Sciences, University of Washington, Seattle, WA; Department of Cardiovascular Research Institute, University of California, San Francisco, CADepartment of Medicine, University of Washington, Seattle, WA; Department of Genome Sciences, University of Washington, Seattle, WA; Department of Cardiovascular Research Institute, University of California, San Francisco, CADepartment of Medicine, University of Washington, Seattle, WA; Department of Genome Sciences, University of Washington, Seattle, WA; Department of Cardiovascular Research Institute, University of California, San Francisco, CADepartment of Medicine, University of Washington, Seattle, WA; Department of Genome Sciences, University of Washington, Seattle, WA; Department of Cardiovascular Research Institute, University of California, San Francisco, CADepartment of Medicine, University of Washington, Seattle, WA; Department of Genome Sciences, University of Washington, Seattle, WA; Department of Cardiovascular Research Institute, University of California, San Francisco, CADepartment of Medicine, University of Washington, Seattle, WA; Department of Genome Sciences, University of Washington, Seattle, WA; Department of Cardiovascular Research Institute, University of California, San Francisco, CADepartment of Medicine, University of Washington, Seattle, WA; Department of Genome Sciences, University of Washington, Seattle, WA; Department of Cardiovascular Research Institute, University of California, San Francisco, CADepartment of Medicine, University of Washington, Seattle, WA; Department of Genome Sciences, University of Washington, Seattle, WA; Department of Cardiovascular Research Institute, University of California, San Francisco, CADepartment of Medicine, University of Washington, Seattle, WA; Department of Genome Sciences, University of Washington, Seattle, WA; Department of Cardiovascular Research Institute, University of California, San Francisco, CAApolipoprotein 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 μg/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 μg/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.http://www.sciencedirect.com/science/article/pii/S0022227520340311diabetes mellituscoronary artery diseaselipidsantioxidant vitaminsstatinsniacin |
| spellingShingle | Timothy S.E. Albert Philippe N. Duchateau Samir S. Deeb Clive R. Pullinger Min H. Cho David C. Heilbron Mary J. Malloy John P. Kane B. Greg Brown Apolipoprotein L-I is positively associated with hyperglycemia and plasma triglycerides in CAD patients with low HDL Journal of Lipid Research diabetes mellitus coronary artery disease lipids antioxidant vitamins statins niacin |
| title | Apolipoprotein L-I is positively associated with hyperglycemia and plasma triglycerides in CAD patients with low HDL |
| title_full | Apolipoprotein L-I is positively associated with hyperglycemia and plasma triglycerides in CAD patients with low HDL |
| title_fullStr | Apolipoprotein L-I is positively associated with hyperglycemia and plasma triglycerides in CAD patients with low HDL |
| title_full_unstemmed | Apolipoprotein L-I is positively associated with hyperglycemia and plasma triglycerides in CAD patients with low HDL |
| title_short | Apolipoprotein L-I is positively associated with hyperglycemia and plasma triglycerides in CAD patients with low HDL |
| title_sort | apolipoprotein l i is positively associated with hyperglycemia and plasma triglycerides in cad patients with low hdl |
| topic | diabetes mellitus coronary artery disease lipids antioxidant vitamins statins niacin |
| url | http://www.sciencedirect.com/science/article/pii/S0022227520340311 |
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