ArticleMolecular and cellular biochemistry2010
Differential response of two models of genetically modified mice fed with high fat and cholesterol diets: relationship to the study of non-alcoholic steatohepatitis.
Article in Molecular and cellular biochemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Deletion of hepatic small heterodimer partner ameliorates development of nonalcoholic steatohepatitis in mice.Journal of lipid research · 2023Article
- Role of Cholesterol-Associated Steatohepatitis in the Development of NASH.Hepatology communications · 2022Review
- Targeting the Inositol Pyrophosphate Biosynthetic Enzymes in Metabolic Diseases.Molecules (Basel, Switzerland) · 2020Review
- Understanding the Impact of Dietary Cholesterol on Chronic Metabolic Diseases through Studies in Rodent Models.Nutrients · 2018Review
- Crossroads between peripheral atherosclerosis, western-type diet and skeletal muscle pathophysiology: emphasis on apolipoprotein E deficiency and peripheral arterial disease.Journal of biomedical science · 2017Review
- 2-heptyl-formononetin increases cholesterol and induces hepatic steatosis in mice.BioMed research international · 2013Article
- Inhibition of bone morphogenetic protein signaling reduces vascular calcification and atherosclerosis.Arteriosclerosis, thrombosis, and vascular biology · 2012Article
- Hepatic overexpression of SIRT1 in mice attenuates endoplasmic reticulum stress and insulin resistance in the liver.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2011Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Research on the molecular basis of the hepatic alterations associated to obesity is dependent on the availability of suitable animal models. Apolipoprotein E deficient mice (ApoE(-/-)) and LDL-receptor deficient mice (LDLr(-/-)) develop steatosis and steatohepatitis when given pro-atherogenic diets. However, previous data suggest that these two models are not completely interchangeable, and that their metabolic phenotype may partially differ in response to nutrient stimuli. The present study further investigates this question, by comparing changes in hepatic inflammation, lipoprotein metabolism, and their related gene expressions. LDLr(-/-) mice were more susceptible to the development of obesity and hepatic steatosis, while the ApoE(-/-) model increased the amount of macrophages and inflammatory nodules in the liver. These changes were accompanied by a differential expression of selected members of the MAPK family and PPARs in the liver.
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Registered trials
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