Autor: |
John W. Gaubatz, Baiba K. Gillard, John B. Massey, Ron C. Hoogeveen, Max Huang, Eric E. Lloyd, Joe L. Raya, Chao-yuh Yang, Henry J. Pownall |
Jazyk: |
angličtina |
Rok vydání: |
2007 |
Předmět: |
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Zdroj: |
Journal of Lipid Research, Vol 48, Iss 2, Pp 348-357 (2007) |
Druh dokumentu: |
article |
ISSN: |
0022-2275 |
DOI: |
10.1194/jlr.M600249-JLR200 |
Popis: |
Small, dense, electronegative low density lipoprotein [LDL(−)] is increased in patients with familial hypercholesterolemia and diabetes, populations at increased risk for coronary artery disease. It is present to a lesser extent in normolipidemic subjects. The mechanistic link between small, dense LDL(−) and atherogenesis is not known. To begin to address this, we studied the composition and dynamics of small, dense LDL(−) from normolipidemic subjects. NEFA levels, which correlate with triglyceride content, are quantitatively linked to LDL electronegativity. Oxidized LDL is not specific to small, dense LDL(−) or lipoprotein [a] (i.e., abnormal lipoprotein). Apolipoprotein C-III is excluded from the most abundant LDL (i.e., that of intermediate density: 1.034 < d < 1.050 g/ml) but associated with both small and large LDL(−). In contrast, lipoprotein-associated phospholipase A2 (LpPLA2) is highly enriched only in small, dense LDL(−). The association of LpPLA2 with LDL may occur through amphipathic helical domains that are displaced from the LDL surface by contraction of the neutral lipid core. |
Databáze: |
Directory of Open Access Journals |
Externí odkaz: |
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