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Increased liver oxidative stress and altered PUFA metabolism precede development of non-alcoholic steatohepatitis in SREBP-1a transgenic spontaneously hypertensive rats with genetic predisposition to hepatic steatosis

Molecular and cellular biochemistry. 2010 Feb ; 335 (1-2) : 119-25. [epub] 20090912

Mol Cell Biochem
ISSN 1573-4919 | 0300-8177
Source

Language English Country Netherlands Media print-electronic

Document type Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't

Persistent link https://www.medvik.cz/link/pmid19756959

Grant support
HL35018 NHLBI NIH HHS - United States
HL56028 NHLBI NIH HHS - United States
HL63709 NHLBI NIH HHS - United States

PubMed 19756959
DOI 10.1007/s11010-009-0248-5
Knihovny.cz E-resources

MeSH
Genetic Predisposition to Disease MeSH
Liver metabolism pathology MeSH
Rats MeSH
Humans MeSH
Fatty Acids, Unsaturated metabolism MeSH
Oxidative Stress * MeSH
Rats, Inbred SHR MeSH
Rats, Transgenic MeSH
Sterol Regulatory Element Binding Protein 1 genetics metabolism MeSH
Fatty Liver genetics metabolism pathology MeSH
Animals MeSH
Check Tag
Rats MeSH
Humans MeSH
Animals MeSH
Publication type
Journal Article MeSH
Research Support, Non-U.S. Gov't MeSH
Research Support, N.I.H., Extramural MeSH
Names of Substances
Fatty Acids, Unsaturated MeSH
Sterol Regulatory Element Binding Protein 1 MeSH
SREBF1 protein, human MeSH Browser

The temporal relationship of hepatic steatosis and changes in liver oxidative stress and fatty acid (FA) composition to the development of non-alcoholic steatohepatitis (NASH) remain to be clearly defined. Recently, we developed an experimental model of hepatic steatosis and NASH, the transgenic spontaneously hypertensive rat (SHR) that overexpresses a dominant positive form of the human SREBP-1a isoform in the liver. These rats are genetically predisposed to hepatic steatosis at a young age that ultimately progresses to NASH in older animals. Young transgenic SHR versus SHR controls exhibited simple hepatic steatosis which was associated with significantly increased hepatic levels of oxidative stress markers, conjugated dienes, and TBARS, with decreased levels of antioxidative enzymes and glutathione and lower concentrations of plasma alpha- and gamma-tocopherol. Transgenic rats exhibited increased plasma levels of saturated FA, decreased levels of n-3 and n-6 polyunsaturated FA (PUFA), and increased n-6/n-3 PUFA ratios. These results are consistent with the hypothesis that excess fat accumulation in the liver in association with increased oxidative stress and disturbances in the metabolism of saturated and unsaturated fatty acids may precede and contribute to the primary pathogenesis of NASH.

Institute for Clinical and Experimental Medicine Prague Czech Republic

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