NONENZYMATIC GLYCOSYLATION OF APOLIPOPROT EIN-A-I AND ITS FUNCTIONAL CONSEQUENCES

Citation
C. Fievet et al., NONENZYMATIC GLYCOSYLATION OF APOLIPOPROT EIN-A-I AND ITS FUNCTIONAL CONSEQUENCES, Diabete et metabolisme, 21(2), 1995, pp. 95-98
Citations number
23
Categorie Soggetti
Endocrynology & Metabolism
Journal title
Diabete et metabolisme
ISSN journal
03381684 → ACNP
Volume
21
Issue
2
Year of publication
1995
Pages
95 - 98
Database
ISI
SICI code
0338-1684(1995)21:2<95:NGOAEA>2.0.ZU;2-7
Abstract
High-density lipoproteins (HDL) are believed to protect against athero sclerosis by promoting the process of reverse cholesterol transport. T his process involves different steps including efflux of cellular chol esterol, cholesterol esterification and lipid transport and exchange. Apolipoprotein-(apo) A-I, the major HDL apolipoprotein, and the HDL-as sociated enzyme lecithin-cholesterol acyltransferase (LCAT), which use s apo A-I as a cofactor play a crucial role in reverse cholesterol tra nsport. HDL may he classified into species according to their apolipop rotein content. Recent data concerning HDL particles indicate that lip oproteins containing apo A-I but not ape A-II (LpA-I) are more effecti ve carriers of free cholesterol and are associated with a protective e ffect agains coronary heart disease. In vitro studies have shown that glycosylated HDL are functionally abnormal and may be considered ather ogenic. Our study considers the different impacts of non-enzymatic gly cosylation of ape A-I or protein-HDL on the reverse cholesterol transp ort process.