| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Papers In Press, published online ahead of print October 26, 2001
UCLA/VA Greater Los Angeles, Los Angeles, CA 90073
Corresponding Author: Reuek{at}ucla.edu
The C57BL/6ByJ (B6By) mouse strain is resistant to diet-induced hypercholesterolemia and atherosclerosis, despite its near genetic identity with the atherosclerosis-susceptible C57BL/6J (B6J) strain. We previously identified a genetic locus, Diet1, which is responsible for the resistant phenotype in B6By mice. To investigate the function of Diet1, we compared mRNA expression profiles in the liver of B6By and B6J mice fed an atherogenic diet using a DNA microarray. These studies revealed elevated expression levels in B6By liver for key bile acid synthesis proteins, including cholesterol 7
J. Biol. Chem, 10.1074/jbc.M107107200
Submitted on July 26, 2001
Revised on October 25, 2001
Accepted on October 25, 2001
The diet1 locus confers protection against hypercholesterolemia through enhanced bile acid metabolism
-hydroxylase and sterol-27-hydroxylase, and the oxysterol nuclear receptor LXR. Expression levels for several other genes involved in bile acid metabolism were subsequently found to differ between B6By and B6J mice, including the bile acid receptor FXR, oxysterol 7-hydroxylase, sterol-12-hydroxylase, and hepatic bile acid transporters on both sinusoidal and canalicular membranes. The overall expression profile of the B6By strain suggests a higher rate of bile acid synthesis and transport in these mice. Consistent with this interpretation, fecal bile acid excretion is increased 2-fold in B6By mice, and bile acid levels in blood and urine are elevated 3-fold and 18-fold, respectively. Genetic analysis of serum bile acid levels revealed co-segregation with Diet1, indicating that this locus is likely responsible for both increased bile acid excretion and resistance to hypercholesterolemia in B6By mice.
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati What's this?
This article has been cited by other articles:
|
|
 |
|
  P. A. Dawson, B. Gardiner, S. Grimmond, and D. Markovich Transcriptional profile reveals altered hepatic lipid and cholesterol metabolism in hyposulfatemic NaS1 null mice Physiol Genomics, September 14, 2006; 26(2): 116 - 124. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. Reue and L. Vergnes Thematic review series: Systems Biology Approaches to Metabolic and Cardiovascular Disorders. Approaches to lipid metabolism gene identification and characterization in the postgenomic era J. Lipid Res., September 1, 2006; 47(9): 1891 - 1907. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C Thomas, J-F Landrier, D Gaillard, J Grober, M-C Monnot, A Athias, and P Besnard Cholesterol dependent downregulation of mouse and human apical sodium dependent bile acid transporter (ASBT) gene expression: molecular mechanism and physiological consequences Gut, September 1, 2006; 55(9): 1321 - 1331. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. Qin, L. A. Borges-Marcucci, M. J. Evans, and D. C. Harnish Bile acid signaling through FXR induces intracellular adhesion molecule-1 expression in mouse liver and human hepatocytes Am J Physiol Gastrointest Liver Physiol, August 1, 2005; 289(2): G267 - G273. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. Vergnes, J. Phan, M. Strauss, S. Tafuri, and K. Reue Cholesterol and Cholate Components of an Atherogenic Diet Induce Distinct Stages of Hepatic Inflammatory Gene Expression J. Biol. Chem., October 31, 2003; 278(44): 42774 - 42784. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| All ASBMB Journals | Molecular and Cellular Proteomics |
| Journal of Lipid Research | ASBMB Today |
