Simple jQuery Dropdowns
Please use this identifier to cite or link to this item: http://repository.li.mahidol.ac.th/dspace/handle/123456789/19776
Title: CD36 and proteoglycan-mediated pathways for (n-3) fatty acid-enriched triglyceride-rich particle blood clearance in mouse models in vivo and in peritoneal macrophages in vitro
Authors: Narumon Densupsoontorn
Yvon A. Carpentier
Radjini Racine
Faith M. Murray
Toru Seo
Rajasekhar Ramakrishnan
Richard J. Deckelbaum
Mahidol University
Université libre de Bruxelles (ULB)
Columbia University, College of Physicians and Surgeons
Keywords: Medicine;Nursing
Issue Date: 1-Feb-2008
Citation: Journal of Nutrition. Vol.138, No.2 (2008), 257-261
Abstract: Because the mechanisms of (n-3) fatty acid-enriched triglyceride-rich particle [(n-3)-TGRP] uptake are not well characterized, we questioned whether (n-3)-TGRP are removed via "nonclassical" pathways, e.g., pathways other than an LDL receptor and/or involving apolipoprotein E (apoE). Chylomicron-sized model (n-3)-TGRP labeled with [3H]cholesteryl ether were injected into wild-type (WT) and CD36 knockout (CD36-/-) mice at low, nonsaturating and high, saturating doses. Blood clearance of (n-3)-TGRP was determined by calculating fractional catabolic rates. At saturating doses, blood clearance of (n-3)-TGRP was slower in CD36-/- mice relative to WT mice, suggesting that in part CD36 contributes to (n-3)-TGRP uptake. To further examine the potential nonclassical clearance pathways, peritoneal-elicited macrophages from WT and CD36-/- mice were incubated with (n-3)-TGRP in the presence of apoE, lactoferrin, and/or sodium chlorate. Cellular (n-3)-TGRP uptake was measured to test the roles of apoE-mediated pathways and/or proteoglycans. ApoE-mediated pathways compensated in part for defective (n-3)-TGRP uptake in CD36-/- cells. Lactoferrin decreased (n-3)-TGRP uptake in the presence of apoE. Inhibition of cell proteoglycan synthesis by chlorate reduced (n-3)-TGRP uptake in both groups of macrophages, and chlorate effects were independent of apoE. We conclude that although CD36 is involved, it is not the primary contributor to the blood clearance of (n-3)-TGRP. The removal of (n-3)-TGRP likely relies more on nonclassical pathways, such as proteoglycan-mediated pathways. © 2008 American Society for Nutrition.
URI: https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=38949113206&origin=inward
http://repository.li.mahidol.ac.th/dspace/handle/123456789/19776
ISSN: 15416100
00223166
Appears in Collections:Scopus 2006-2010

Files in This Item:
There are no files associated with this item.


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.