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J. Lipid Res.
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A more recent version of this article appeared on October 1, 2009

Papers In Press, published online ahead of print March 17, 2009
J. Lipid Res., doi:10.1194/jlr.M900022-JLR200
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Submitted on January 21, 2009
Revised on March 9, 2009
Accepted on March 13, 2009

Dietary sucrose is essential to the development of liver injury in the MCD model of steatohepatitis

Michael K. Pickens, Jim S. Yan, Raymond K. Ng, Hisanobu Ogata, James P. Grenert, Carine Beysen, Scott M. Turner, and Jacquelyn J. Maher

Medicine, University of California, San Francisco, San Francisco, CA 94110

Corresponding Author: jmaher{at}medsfgh.ucsf.edu

Methionine-choline-deficient (MCD) diets cause steatohepatitis in rodents and are used to study the pathophysiology of fatty liver disease in human beings. The most widely-used commercial MCD formulas not only lack methionine and choline, but also contain excess sucrose and fat. The objective of this study was to determine whether dietary sucrose in the MCD formula plays a role in the pathogenesis of MCD-related liver disease. We prepared two custom MCD formulas, one containing sucrose as the principal carbohydrate and the other substituting sucrose with starch. Mice fed the sucrose-enriched formula developed typical features of MCD-related liver disease including hepatic steatosis, hepatocellular apoptosis, ALT elevation, lipid peroxidation and hepatic inflammation. In contrast, mice fed MCD-starch were significantly protected against liver injury. MCD-sucrose and MCD-starch mice displayed identical diet-related abnormalities in hepatic fatty acid uptake and triglyceride secretion. Hepatic de novo lipogenesis and triglyceride synthesis, however, were 2 times higher in MCD-sucrose mice than MCD-starch mice (P < 0.01). Hepatic lipid analysis revealed accumulation of excess saturated fatty acids in MCD-sucrose mice that correlated with hepatocellular injury. Overall, the results indicate that dietary sucrose is critical to the pathogenesis of MCD-mediated steatohepatitis. They suggest that saturated fatty acids, which are products of de novo lipogenesis, are mediators of hepatic toxicity in this model of liver disease.


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