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Model of non-alcoholic fatty liver disease in rats for toxicological studies.
Autoři: Kučera Otto | Křiváková Pavla | Roušar Tomáš | Lotková Halka | Červinková Zuzana
Rok: 2008
Druh publikace: článek ve sborníku
Název zdroje: Toxicology Letters
Název nakladatele: Elsevier Ireland Ltd
Místo vydání: Shannon
Strana od-do: 51
Tituly:
Jazyk Název Abstrakt Klíčová slova
cze NAFLD model u krys a jeho použití při toxikologických studiích NAFLD model u krys a jeho použití při toxikologických studiích
eng Model of non-alcoholic fatty liver disease in rats for toxicological studies. Nonalcoholic fatty liver disease (NAFLD) is an important cause of liver-related morbidity and mortality. NAFLD is often the hepatic manifestation of metabolic syndrome and represents a wide spectrum of conditions ranging from nonprogressive hepatic steatosis, to nonalcoholic steatohepatitis that may progress to cirrhosis and end-stage liver disease. The aim of this project is to establish and characterize a nutritional model of NAFLD on rats. This model will be used for comparison of toxic effects of model hepatotoxins on intact liver and liver affected by NAFLD. Wistar male rats were fed ad libitum a standard pelleted diet (ST-1, 10% of energy from fat); low-fat liquid diet (LFLD, 35% of energy from fat) and high-fat liquid diet (HFLD, 71% of energy from fat) for 3 weeks. Then serum ALT, AST, glycaemia, levels of triacylglycerols and cholesterol were measured. Respiration of isolated liver mitochondria was assessed using high-resolution respirometry. Malondialdehyde content in the liver and tissue cytokines (TNF-&#61537;, IL-6, TGF-&#61538;) were measured and histopathological samples were prepared (H+E, Sudan III). Feeding with HFLD (less in LFLD) induced periportal small-droplet steatosis with mild focal inflammation without necrosis in comparison with control group (ST-1). There were no significant differences among groups in serum biochemical parameters except lower concentration of triacylglycerols in LFLD against ST-1 (p<0.05). We found a significant decrease in activity of respiratory complex I in LFLD and HFLD groups and increase in tissue TNF-&#61537; and IL-6 in HFLD in comparison with ST-1 (p<0.05). NAFLD, hepatotoxicity, steatohepatitis.