AJP - Endo Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Endocrinol Metab 291: E755-E760, 2006. First published May 9, 2006; doi:10.1152/ajpendo.00111.2006
0193-1849/06 $8.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow A corrigendum has been published
Right arrow All Versions of this Article:
291/4/E755    most recent
00111.2006v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (4)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Noh, H.-L.
Right arrow Articles by Goldberg, I. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Noh, H.-L.
Right arrow Articles by Goldberg, I. J.

Acute lipoprotein lipase deletion in adult mice leads to dyslipidemia and cardiac dysfunction

Hye-Lim Noh,1 Kazue Okajima,2 Jeffery D. Molkentin,3 Sunichi Homma,2 and Ira J. Goldberg1,2

1Divisions of Preventive Medicine and Nutrition, and 2Cardiology, Columbia University College of Physicians and Surgeons, New York, New York; 3Department of Pediatrics, University of Cincinnati, Children's Hospital Medical Center, Division of Molecular Cardiovascular Biology, Cincinnati, Ohio

Submitted 9 March 2006 ; accepted in final form 27 April 2006

The most energy-requiring organ in the body, the cardiac muscle, relies primarily on lipoprotein-derived fatty acids. Prenatal loss of cardiac lipoprotein lipase (LPL) leads to hypertriglyceridemia, but no cardiac dysfunction, in young mice. Cardiac specific loss of LPL in 8-wk-old mice was produced by a 2-wk tamoxifen treatment of MerCreMer (MCM)/Lplflox/flox mice. LPL gene deletion was confirmed by PCR analysis, and LPL mRNA expression was reduced by ~70%. One week after tamoxifen was completed, triglyceride was increased with LPL deletion, 162 ± 53 vs. 91 ± 21 mg/dl, P < 0.01. Tamoxifen treatment of Lplflox/flox mice did not cause a significant increase in triglyceride levels. Four weeks after tamoxifen, MCM/Lplflox/flox mice had triglyceride levels of 190 ± 27 mg/dl, similar to those of mice with prenatal LPL deletion. One week after the tamoxifen, MCM/Lplflox/flox, but not Lplflox/flox, mice had decreases in carnitine palmitoyl transferase I mRNA (18%) and pyruvate dehydrogenase kinase 4 mRNA (38%). These changes in gene expression became more robust with time. Acute loss of LPL decreased ejection fraction and increased mRNA levels for atrial natriuretic factor. Our studies show that acute loss of LPL can be produced and leads to rapid alteration in gene expression and cardiac dysfunction.

triglyceride; tamoxifen; hypertriglyceridemia; peroxisome proliferator-activated receptor; heart failure; cardiac energetics


Address for reprint requests and other correspondence: I. J. Goldberg, Dept. of Medicine, Columbia University, 630 West 168th St., New York, NY 10032 (e-mail: ijg3{at}columbia.edu)




This article has been cited by other articles:


Home page
 Br J AnaesthHome page
R. D. Evans and Y. Niu
Hypolipidaemic effects of high-dose insulin therapy
Br. J. Anaesth., April 1, 2008; 100(4): 429 - 433.
[Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online
Copyright © 2006 by the American Physiological Society.