|
|
||||||||
Journal of Lipid Research, Vol 36, 1813-1824, Copyright © 1995 by Lipid Research, Inc.
M Liu, JD Bagdade and PV Subbaiah
To determine whether the specificity of lecithin: cholesterol
acyltransferase (LCAT) influences the susceptibility to atherosclerosis, we
compared the composition and in vitro synthesis of cholesteryl ester (CE)
in the plasmas of 14 vertebrate species with varying predisposition to
atherosclerosis. The susceptible species (Group I) had significantly higher
ratios of 16:0 CE/20:4 CE in their plasma than the resistant species (Group
II). The in vitro formation of labeled CE species in native plasma from
labeled cholesterol correlated highly with the mass composition, showing
that the LCAT reaction is the predominant source of plasma CE in all the
animal species examined. Isolated LCATs from Group I species also
synthesized CE with higher ratios of 16:0/20:4 than LCATs from Group II
when egg phosphatidylcholine (PC) was used as the acyl donor. In addition,
the Group I LCATs exhibited lower specificity towards sn-2-20:4 and sn-2-
22:6 PCs, and higher specificity towards sn-2-18:2 PC species than Group II
LCATs. With 16:0-20:4 PC as the substrate, all Group I LCATs synthesized
more 16:0 CE than 20:4 CE, whereas all Group II LCATs, with the exception
of dog enzyme, synthesized predominantly 20:4 CE, showing that the two
types of LCAT have different positional specificities towards this PC.
These results suggest that there are two classes of LCAT in nature that
differ from each other in their substrate and positional specificities,
possibly because of differences in their active-site architectures. We
propose that the presence of one type of LCAT, which cannot efficiently
transfer certain long chain polyunsaturated acyl groups and which
consequently synthesizes more saturated CE, may increase the risk of
atherosclerosis.
ARTICLES
Specificity of lecithin:cholesterol acyltransferase and atherogenic risk: comparative studies on the plasma composition and in vitro synthesis of cholesteryl esters in 14 vertebrate species
Department of Medicine, Rush Medical College, Chicago, IL 60612, USA.
![]()
CiteULike
Complore
Connotea
Del.icio.us
Digg
Reddit
Technorati What's this?
This article has been cited by other articles:
![]() |
A. Yesilaltay, M. G. Morales, L. Amigo, S. Zanlungo, A. Rigotti, S. L. Karackattu, M. H. Donahee, K. F. Kozarsky, and M. Krieger Effects of Hepatic Expression of the High-Density Lipoprotein Receptor SR-BI on Lipoprotein Metabolism and Female Fertility Endocrinology, April 1, 2006; 147(4): 1577 - 1588. [Abstract] [Full Text] [PDF] |
||||
![]() |
Y. Zhao, A. K. Gebre, and J. S. Parks Amino acids 149 and 294 of human lecithin:cholesterol acyltransferase affect fatty acyl specificity J. Lipid Res., December 1, 2004; 45(12): 2310 - 2316. [Abstract] [Full Text] [PDF] |
||||
![]() |
P. V. Subbaiah, J. M. Sowa, and M. H. Davidson Evidence for altered positional specificity of LCAT in vivo: studies with docosahexaenoic acid feeding in humans J. Lipid Res., December 1, 2004; 45(12): 2245 - 2251. [Abstract] [Full Text] [PDF] |
||||
![]() |
L. Zhou and A. Nilsson Sources of eicosanoid precursor fatty acid pools in tissues J. Lipid Res., October 1, 2001; 42(10): 1521 - 1542. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. W. Furbee Jr., O. Francone, and J. S. Parks Alteration of plasma HDL cholesteryl ester composition with transgenic expression of a point mutation (E149A) of human LCAT J. Lipid Res., October 1, 2001; 42(10): 1626 - 1635. [Abstract] [Full Text] [PDF] |
||||
![]() |
P. V. Subbaiah, V. S. Subramanian, and M. Liu Trans unsaturated fatty acids inhibit lecithin: cholesterol acyltransferase and alter its positional specificity J. Lipid Res., July 1, 1998; 39(7): 1438 - 1447. [Abstract] [Full Text] |
||||
![]() |
M. Liu, R. W. St. Clair, and P. V. Subbaiah Impaired function of lecithin:cholesterol acyltransferase in atherosclerosis-susceptible White Carneau pigeons: possible effects on metabolism of oxidized phospholipids J. Lipid Res., February 1, 1998; 39(2): 245 - 254. [Abstract] [Full Text] |
||||
![]() |
S. M. Innis and R. Dyer Dietary Triacylglycerols with Palmitic Acid (16:0) in the 2-Position Increase 16:0 in the 2-Position of Plasma and Chylomicron Triacylglycerols, but Reduce Phospholipid Arachidonic and Docosahexaenoic Acids, and Alter Cholesteryl Ester Metabolism in Formula-Fed Piglets J. Nutr., July 1, 1997; 127(7): 1311 - 1319. [Abstract] [Full Text] |
||||
![]() |
J. Wang, A. K. Gebre, R. A. Anderson, and J. S. Parks Amino Acid Residue 149of Lecithin:Cholesterol Acyltransferase Determines Phospholipase A2 and Transacylase Fatty Acyl Specificity J. Biol. Chem., January 3, 1997; 272(1): 280 - 286. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. Seguret-Mace, M. Latta-Mahieu, G. Castro, G. Luc, J.-C. Fruchart, E. Rubin, P. Denefle, and N. Duverger Potential Gene Therapy for Lecithin-Cholesterol Acyltransferase (LCAT)–Deficient and Hypoalphalipoproteinemic Patients With Adenovirus-Mediated Transfer of Human LCAT Gene Circulation, November 1, 1996; 94(9): 2177 - 2184. [Abstract] [Full Text] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| All ASBMB Journals | Journal of Biological Chemistry |
| Molecular and Cellular Proteomics | ASBMB Today |