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SHR Neuro Krebs Kardio Lipid Stoffw Microb

Fengler, VH; Macheiner, T; Kessler, SM; Czepukojc, B; Gemperlein, K; Müller, R; Kiemer, AK; Magnes, C; Haybaeck, J; Lackner, C; Sargsyan, K.
Susceptibility of Different Mouse Wild Type Strains to Develop Diet-Induced NAFLD/AFLD-Associated Liver Disease.
PLoS One. 2016; 11(5):e0155163-e0155163 Doi: 10.1371/journal.pone.0155163 [OPEN ACCESS]
Web of Science PubMed PUBMED Central FullText FullText_MUG

 

Führende Autor*innen der Med Uni Graz
Fengler Vera
Sargsyan Karine
Co-Autor*innen der Med Uni Graz
Haybäck Johannes
Kessler Sonja
Lackner Karoline
Macheiner Tanja
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Abstract:
Although non-alcoholic and alcoholic fatty liver disease have been intensively studied, concerning pathophysiological mechanisms are still incompletely understood. This may be due to the use of different animal models and resulting model-associated variation. Therefore, this study aimed to compare three frequently used wild type mouse strains in their susceptibility to develop diet-induced features of non-alcoholic/alcoholic fatty liver disease. Fatty liver disease associated clinical, biochemical, and histological features in C57BL/6, CD-1, and 129Sv WT mice were induced by (i) high-fat diet feeding, (ii) ethanol feeding only, and (iii) the combination of high-fat diet and ethanol feeding. Hepatic and subcutaneous adipose lipid profiles were compared in CD-1 and 129Sv mice. Additionally hepatic fatty acid composition was determined in 129Sv mice. In C57BL/6 mice dietary regimens resulted in heterogeneous hepatic responses, ranging from pronounced steatosis and inflammation to a lack of any features of fatty liver disease. Liver-related serum biochemistry showed high deviations within the regimen groups. CD-1 mice did not exhibit significant changes in metabolic and liver markers and developed no significant steatosis or inflammation as a response to dietary regimens. Although 129Sv mice showed no weight gain, this strain achieved most consistent features of fatty liver disease, apparent from concentration alterations of liver-related serum biochemistry as well as moderate steatosis and inflammation as a result of all dietary regimens. Furthermore, the hepatic lipid profile as well as the fatty acid composition of 129Sv mice were considerably altered, upon feeding the different dietary regimens. Accordingly, diet-induced non-alcoholic/alcoholic fatty liver disease is most consistently promoted in 129Sv mice compared to C57BL/6 and CD-1 mice. As a conclusion, this study demonstrates the importance of genetic background of used mouse strains for modeling diet-induced non-alcoholic/alcoholic fatty liver disease.
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Animals -
Aspartate Aminotransferases - metabolism
Biomarkers - metabolism
Cholesterol - metabolism
Diet, High-Fat - adverse effects
Dietary Fats - administration & dosage
Disease Models, Animal -
Disease Susceptibility -
Ethanol - administration & dosage
Fatty Acids, Nonesterified - metabolism
Fatty Liver, Alcoholic - etiology
Fatty Liver, Alcoholic - genetics
Fatty Liver, Alcoholic - metabolism
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Liver - metabolism
Liver - pathology
Liver Function Tests -
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Mice -
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Mice, Inbred C57BL -
Mice, Inbred Strains -
Non-alcoholic Fatty Liver Disease - etiology
Non-alcoholic Fatty Liver Disease - genetics
Non-alcoholic Fatty Liver Disease - metabolism
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