| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
Papers In Press, published online ahead of print October 1, 2004
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Medicine Dept., Division of Cardiology, University of California at Los Angeles, Los Angeles, CA 90095
Corresponding Author: lcastellani{at}mednet.ucla.edu
We previously demonstrated that transgenic mice overexpressing mouse apolipoprotein AII (apoAII) exhibit several traits associated with the insulin resistance (IR) syndrome, including increased atherosclerosis, hypertriglyceridemia, obesity, and IR. The skeletal muscle (SM) appeared to be the IR tissue in the apoAII transgenic (apoAIItg) mice. We now demonstrate a decrease in fatty acid (FA) oxidation in SM of apoAIItg mice, consistent with reports that decreased SM FA oxidation is associated with increased SM triglyceride accumulation, SM IR, and obesity. The decrease in FA oxidation is not due to decreased carnitine palmitoyltransferase-1 activity, since oxidation of palmitate and octanoate were similarly decreased. Quantitative RT-PCR analysis of gene expression demonstrated that the decrease in FA oxidation may be explained by a decrease in medium chain acyl-CoA dehydrogenase. We previously demonstrated that HDL from apoAIItg mice exhibit reduced binding to CD36, a scavenger receptor involved in FA metabolism. However, studies of combined apoAIItg and CD36 knockout mice suggest that the major effects of apoAII are independent of CD36. Rosiglitazone treatment significantly ameliorated IR in the apoAIItg mice, suggesting that the underlying mechanisms of IR in this animal model may share common features with certain types of human IR.
Revised on October 1, 2004
Accepted on September 20, 2004
Mechanisms mediating insulin resistance in transgenic mice overexpressing mouse apolipoprotein A-II
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati What's this?
This article has been cited by other articles:
|
|
 |
|
  L. W. Castellani, C. N. Nguyen, S. Charugundla, M. M. Weinstein, C. X. Doan, W. S. Blaner, N. Wongsiriroj, and A. J. Lusis Apolipoprotein AII Is a Regulator of Very Low Density Lipoprotein Metabolism and Insulin Resistance J. Biol. Chem., April 25, 2008; 283(17): 11633 - 11644. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. W. Castellani, J. J. Chang, X. Wang, A. J. Lusis, and W. F. Reynolds Transgenic mice express human MPO -463G/A alleles at atherosclerotic lesions, developing hyperlipidemia and obesity in -463G males J. Lipid Res., July 1, 2006; 47(7): 1366 - 1377. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Z. Su, Y. Li, J. C. James, A. H. Matsumoto, G. A. Helm, A. J. Lusis, and W. Shi Genetic linkage of hyperglycemia, body weight and serum amyloid-P in an intercross between C57BL/6 and C3H apolipoprotein E-deficient mice Hum. Mol. Genet., May 15, 2006; 15(10): 1650 - 1658. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. M. Arbones-Mainar, M. A. Navarro, S. Acin, M. A. Guzman, C. Arnal, J. C. Surra, R. Carnicer, H. M. Roche, and J. Osada Trans-10, cis-12- and cis-9, trans-11-Conjugated Linoleic Acid Isomers Selectively Modify HDL-Apolipoprotein Composition in Apolipoprotein E Knockout Mice J. Nutr., February 1, 2006; 136(2): 353 - 359. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. O. Goodarzi, H. Wong, M. J. Quinones, K. D. Taylor, X. Guo, L. W. Castellani, H. J. Antoine, H. Yang, W. A. Hsueh, and J. I. Rotter The 3' Untranslated Region of the Lipoprotein Lipase Gene: Haplotype Structure and Association with Post-Heparin Plasma Lipase Activity J. Clin. Endocrinol. Metab., August 1, 2005; 90(8): 4816 - 4823. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| All ASBMB Journals | Journal of Biological Chemistry |
| Molecular and Cellular Proteomics | ASBMB Today |
