| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Correspondence to:
John S. Parks, To whom correspondence should be addressed., jparks{at}wfubmc.edu (E-mail)
Previous studies have indicated that LCAT may play a role in the generation of cholesteryl esters (CE) in plasma apolipoprotein B (apoB) lipoproteins. The purpose of the present study was to examine the quantitative importance of LCAT on apoB lipoprotein CE fatty acid (CEFA) composition. LCAT-/- mice were crossed into the LDL receptor (LDLr)-/- and apoE-/- background to retard the clearance and increase the concentration of apoB lipoprotein in plasma. Plasma free cholesterol was significantly elevated but total and esterified cholesterol concentrations were not significantly affected by removal of functioning LCAT in either the LDLr-/- or apoE-/- mice consuming a chow diet. However, when functional LCAT was removed from LDLr-/- mice, the CEFA ratio (saturated + monounsaturated/polyunsaturated) of plasma LDL increased 7-fold because of a 2-fold increase in saturated and monounsaturated CE, a 40% reduction in cholesteryl linoleate, and a complete absence of long chain (>18 carbon) polyunsaturated CE (20:4, 20:5n-3, and 22:6n-3), from 29.3% to 0%. Removal of functional LCAT from apoE-/- mice resulted in only a 1.6-fold increase in the CEFA ratio, due primarily to a complete elimination of long chain CE (7.7% to 0%).
Our results demonstrate that LCAT contributes significantly to the CEFA pool of apoB lipoprotein and is the only source of plasma long chain polyunsaturated CE in these mice. — Furbee, J. W., Jr., O. Francone, and J. S. Parks. In vivo contribution of LCAT to apolipoprotein B lipoprotein cholesteryl esters in LDL receptor and apolipoprotein E knockout mice. J. Lipid Res. 2002. 43: 428–437.
Supplementary key words:
mouse, high density lipoprotein, low density lipoprotein, VLDL, chylomicron remnant, ACAT, polyunsaturated fatty acids, lecithin:cholesterol acyltransferase
Copyright © 2002 by Lipid Research, Inc.
In vivo contribution of LCAT to apolipoprotein B lipoprotein cholesteryl esters in LDL receptor and apolipoprotein E knockout mice
James W. Furbee, Jr.a,
Omar Franconeb, and
John S. Parksa
a Department of Pathology, Section on Comparative Medicine, Wake Forest University School of Medicine, Medical Center Blvd., Winston-Salem, NC 27157-1040
b Pfizer, Inc., Groton, CT 06340
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati What's this?
This article has been cited by other articles:
|
|
 |
|
  X. Zhu, J.-Y. Lee, J. M. Timmins, J. M. Brown, E. Boudyguina, A. Mulya, A. K. Gebre, M. C. Willingham, E. M. Hiltbold, N. Mishra, et al. Increased Cellular Free Cholesterol in Macrophage-specific Abca1 Knock-out Mice Enhances Pro-inflammatory Response of Macrophages J. Biol. Chem., August 22, 2008; 283(34): 22930 - 22941. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. Li, M. Naples, H. Song, R. Yuan, F. Ye, S. Shafi, K. Adeli, and D. S. Ng LCAT-null mice develop improved hepatic insulin sensitivity through altered regulation of transcription factors and suppressors of cytokine signaling Am J Physiol Endocrinol Metab, August 1, 2007; 293(2): E587 - E594. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. W. Joyce, E. M. Wagner, F. Basso, M. J. Amar, L. A. Freeman, R. D. Shamburek, C. L. Knapper, J. Syed, J. Wu, B. L. Vaisman, et al. ABCA1 Overexpression in the Liver of LDLr-KO Mice Leads to Accumulation of Pro-atherogenic Lipoproteins and Enhanced Atherosclerosis J. Biol. Chem., November 3, 2006; 281(44): 33053 - 33065. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. Song, L. Zhu, C. M. Picardo, G. Maguire, V. Leung, P. W. Connelly, and D. S. Ng Coordinated alteration of hepatic gene expression in fatty acid and triglyceride synthesis in LCAT-null mice is associated with altered PUFA metabolism Am J Physiol Endocrinol Metab, January 1, 2006; 290(1): E17 - E25. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. G. Lee, R. Shah, J. K. Sawyer, R. L. Hamilton, J. S. Parks, and L. L. Rudel ACAT2 contributes cholesteryl esters to newly secreted VLDL, whereas LCAT adds cholesteryl ester to LDL in mice J. Lipid Res., June 1, 2005; 46(6): 1205 - 1212. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. G. Lee, K. L. Kelley, J. K. Sawyer, R. V. Farese Jr, J. S. Parks, and L. L. Rudel Plasma Cholesteryl Esters Provided by Lecithin:Cholesterol Acyltransferase and Acyl-Coenzyme A:Cholesterol Acyltransferase 2 Have Opposite Atherosclerotic Potential Circ. Res., November 12, 2004; 95(10): 998 - 1004. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J.-Y. Lee, L. Lanningham-Foster, E. Y. Boudyguina, T. L. Smith, E. R. Young, P. L. Colvin, M. J. Thomas, and J. S. Parks Pre{beta} high density lipoprotein has two metabolic fates in human apolipoprotein A-I transgenic mice J. Lipid Res., April 1, 2004; 45(4): 716 - 728. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. S. Ng, C. Xie, G. F. Maguire, X. Zhu, F. Ugwu, E. Lam, and P. W. Connelly Hypertriglyceridemia in Lecithin-cholesterol Acyltransferase-deficient Mice Is Associated with Hepatic Overproduction of Triglycerides, Increased Lipogenesis, and Improved Glucose Tolerance J. Biol. Chem., February 27, 2004; 279(9): 7636 - 7642. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Z. Chen, R. L. Fitzgerald, J. E. Saffitz, C. F. Semenkovich, and G. Schonfeld Amino Terminal 38.9% of Apolipoprotein B-100 Is Sufficient to Support Cholesterol-Rich Lipoprotein Production and Atherosclerosis Arterioscler. Thromb. Vasc. Biol., April 1, 2003; 23(4): 668 - 674. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. L. Willner, B. Tow, K. K. Buhman, M. Wilson, D. A. Sanan, L. L. Rudel, and R. V. Farese Jr. Deficiency of acyl CoA:cholesterol acyltransferase 2 prevents atherosclerosis in apolipoprotein E-deficient mice PNAS, February 4, 2003; 100(3): 1262 - 1267. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| All ASBMB Journals | Journal of Biological Chemistry |
| Molecular and Cellular Proteomics | ASBMB Today |
