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Published bySamuel Valente Bergler Modified over 6 years ago
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Levels of prebeta-1 high-density lipoprotein are elevated in 3 phenotypes of dyslipidemia
Eveline Oestreicher Stock, MD, Christine T. Ferrara, MD, PhD, Patricia M. O'Connor, MD, Josefina M. Naya-Vigne, MD, Philip H. Frost, MD, Mary J. Malloy, MD, John P. Kane, MD, PhD, Clive R. Pullinger, PhD Journal of Clinical Lipidology Volume 12, Issue 1, Pages (January 2018) DOI: /j.jacl Copyright © 2017 National Lipid Association Terms and Conditions
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Journal of Clinical Lipidology 2018 12, 99-109DOI: (10. 1016/j. jacl
Copyright © 2017 National Lipid Association Terms and Conditions
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Figure 1 Increases in absolute levels of prebeta-1 HDL (mg apoA-1/dL) in 3 groups of dyslipidemic patients compared to a control, normolipidemic group. The increases were statistically significant in all 3 cases as determined by the independent t-test. Values were log transformed before testing. Journal of Clinical Lipidology , DOI: ( /j.jacl ) Copyright © 2017 National Lipid Association Terms and Conditions
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Figure 2 The prebeta-1 HDL cycle. The balance between rates of formation and removal determine the steady-state concentration of prebeta-1 HDL in plasma. After accepting unesterified cholesterol via ABCA1-mediated efflux, the prebeta-1 HDL particles are converted into larger alpha HDL by the esterifying action of the enzyme lecithin-cholesterol acyltransferase (LCAT) that forms more hydrophobic cholesteryl esters. The alpha HDL particles can be remodeled by the action of cholesteryl ester transfer protein (CETP), phospholipid transfer protein (PLTP), and hepatic lipase (HL), and in the process prebeta-1 HDL is regenerated. During this process cholesteryl esters are transferred from alpha HDL to apoB-containing lipoproteins (chylomicrons, VLDL, intermediate-density lipoproteins, and LDL). CETP also transfers triglycerides from the apoB-containing lipoproteins to alpha HDL. Prebeta-1 HDL is also generated during the selective uptake of cholesteryl esters from alpha HDL by the liver via the scavenger receptor class B type I (SR-B1) and from apoA-1 synthesized de novo and secreted by the liver. Journal of Clinical Lipidology , DOI: ( /j.jacl ) Copyright © 2017 National Lipid Association Terms and Conditions
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