J. Lipid Res. Neurobiology of Lipids (ISSN1683-5506)
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
QUICK SEARCH:   [advanced]


     

A more recent version of this article appeared on January 1, 2007

Papers In Press, published online ahead of print October 3, 2006
J. Lipid Res., doi:10.1194/jlr.M600384-JLR200
This Article
Right arrow Full Text (Accepted Manuscript)
Right arrow All Versions of this Article:
M600384-JLR200v1
48/1/145    most recent
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 Google Scholar
Google Scholar
Right arrow Articles by Pulawa, L. K.
Right arrow Articles by Eckel, R. H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Pulawa, L. K.
Right arrow Articles by Eckel, R. H.
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?

Submitted on August 28, 2006
Accepted on October 3, 2006

Dose-dependent reduction of plasma triglycerides in apolipoprotein CII transgenic mice with skeletal muscle specific overexpression of lipoprotein lipase

Leslie K. Pulawa, Dalan R. Jensen, Alison Coates, and Robert H. Eckel

Division of Endocrinology, Metabolism and Diabetes, University of Colorado at Denver and Health Sciences Center, Aurora, CO 80045

Corresponding Author: leslie.pulawa{at}uchsc.edu

Lipoprotein lipase (LPL) and its specific physiological activator, apolipoprotein CII (apoCII), regulate the hydrolysis of triglycerides (TG) from circulating TG-rich lipoproteins. Previously we developed a skeletal muscle-specific LPL transgenic mouse that had lower plasma TG. ApoCII transgenic mice develop hypertriglyceridemia attributed to delayed clearance. To investigate whether overexpression of LPL could correct this apoCII induced hypertriglyceridemia, mice with overexpression of human apoCII (CII) were crossbred with mice with two levels of muscle-specific human LPL overexpression (LPL-L or LPL-H). Plasma TG levels were 319 ± 39 mg/dl in CII mice and 39 ± 5 mg/dl in wildtype mice. Compared to CII mice, apoCII transgenic mice with the higher level of LPL overexpression (CIILPL-H) had a 50% reduction in plasma TG levels (p=0.013). Heart LPL activity was reduced by approximately 30% in mice with the human apoCII transgene which accompanied a more modest 10% decrease in total LPL protein. Overexpression of human LPL in skeletal muscle resulted in dose-dependent reduction of plasma triglycerides in apoCII transgenic mice. Along with plasma apoCII concentrations, heart and skeletal muscle LPL activities were predictors of plasma TG. These data suggest that mice with the human apoCII transgene may have alterations in the expression/activity of the endogenous LPL in the heart. Furthermore, the decrease of LPL activity in the heart, along with the inhibitory effects of excess apoCII, may contribute to the hypertriglyceridemia observed in apoCII transgenic mice.


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?




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
 All ASBMB Journals   Journal of Biological Chemistry 
 Molecular and Cellular Proteomics   ASBMB Today 
Copyright © 2006 by the American Society for Biochemistry and Molecular Biology.