J. Lipid Res. Acyl Labeled PIP's available August 1, 2008
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by de la Llera, M.
Right arrow Articles by Rothblat, G.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by de la Llera, M.
Right arrow Articles by Rothblat, G.
Social Bookmarking
 Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

Journal of Lipid Research, Vol 22, 245-253, Copyright © 1981 by Lipid Research, Inc.


ARTICLES

Mechanism of triglyceride accumulation in rat preadipocyte cultures exposed to very low density lipoprotein

M de la Llera, JM Glick and G Rothblat

Cultured preadipocytes derived from the stromal-vascular fraction of adipose tissue have been shown to accumulate sufficient triglycerides to assume adipocyte morphology when exposed to high concentrations of very low density lipoprotein. Since these cells synthesize and secrete lipoprotein lipase it was of interest to determine whether the accumulation of intracellular triglyceride originated from the uptake of products of the lipase reaction or whether the cells were utilizing intact lipoprotein particles. Upon incubation of preadipocytes with very low density lipoprotein, the triglyceride disappeared from the medium and accumulated in the cells. This response was accentuated by the addition of heparin to the culture medium. Balance studies conducted in the presence of heparin demonstrated that the loss of medium triglyceride could account for the increase in cell stores. Quantitative studies demonstrated that the increase in cellular triglyceride was a result of the cellular uptake and reesterification of the fatty acids liberated from very low density lipoprotein triglycerides by the action of cellular lipoprotein lipase. The magnitude of the cellular response was dependent on the concentration of fetal bovine serum in the incubation medium and increased as the serum level decreased. Likewise, when albumin was substituted for the serum, increasing amounts of albumin decreased the cellular triglyceride accumulation. It was concluded that the presence of albumin in the culture medium modulated cellular triglyceride accumulation by 1) influencing the extent of triglyceride lipolysis and 2) by regulating the uptake of liberated fatty acid into the cells. Experiments using very low density lipoprotein containing radiolabeled triglyceride and cholesteryl esters demonstrated that the uptake of the very low density lipoprotein or the remnant particle produced by the action of lipase did not significantly contribute to the accumulation of triglyceride in the cells.
Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?


This article has been cited by other articles:


Home page
Arterioscler. Thromb. Vasc. Bio.Home page
T. Chiba, T. Nakazawa, K. Yui, E. Kaneko, and K. Shimokado
VLDL Induces Adipocyte Differentiation in ApoE-Dependent Manner
Arterioscler. Thromb. Vasc. Biol., August 1, 2003; 23(8): 1423 - 1429.
[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 
Copyright © 1981 by the American Society for Biochemistry and Molecular Biology.