Nonalcoholic fatty liver disease in AxB mice
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE26225 | GEO | 2011/01/05
SECONDARY ACCESSION(S): PRJNA134987
REPOSITORIES: GEO
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2023-04-30 | E-MTAB-11980 | biostudies-arrayexpress
Project description:Background & Aims: Overnutrition is one of the major causes of non-alcoholic fatty liver disease (NAFLD) and its advanced form non-alcoholic steatohepatitis (NASH). Besides the quantity of consumed calories, distinct dietary components are increasingly recognized as important contributor to the pathogenesis of NASH. We aimed to develop and characterize a hitherto missing murine model which resembles both the pathology and nutritional situation of NASH-patients in Western societies. Methods: We developed a NASH-inducing diet (ND) enriched with sucrose, cholesterol and a high concentration of fats rich in saturated fatty acids in a composition which mimics Western food. C57Bl6/N mice were fed with the ND or control chow for 12 weeks. Biochemical, real-time polymerase chain reaction, Western Blot and immunohistochemical analyses were performed to characterize systemic and hepatic changes induced by ND-feeding. Immunohistochemistry was used to assess c-Jun levels and activation in 110 human NAFLD and control liver specimens applying tissue micro array technology. Results: ND-fed mice showed significant body weight gain, impaired glucose tolerance, elevated fasting blood glucose levels as well as decreased adiponectin and increased leptin serum levels compared to control mice. In the liver, ND-feeding led to marked steatosis, enhanced cholesterol levels, distinct signs of oxidative stress, hepatocellular damage, inflammation, activation of hepatic stellate cells, and beginning fibrosis. Transcriptome-wide hepatic gene expression analysis comparing ND-fed mice and control mice indicated main alterations in lipid metabolism and inflammatory processes. Search for over-represented transcription factor target sites among the differentially expressed genes identified AP-1 as the most likely factor to cause the transcriptional changes in ND-livers. Combining differentially expressed gene and protein-protein interaction network analysis identified c-Jun (a component of the AP-1 complex) as hub in the largest connected deregulated sub-network in ND-livers. In accordance, ND-livers revealed c-Jun-phosphorylation and nuclear translocation. Moreover, hepatic c-Jun RNA and protein expression was enhanced in ND-fed compared to control mice. Also NAFLD-patients showed enhanced hepatic c-Jun levels, which correlated with inflammation, and notably, with the degree of hepatic steatosis. Conclusions: The new dietary mouse-model shows important pathological changes also found in human NASH and indicates c-jun/AP-1 activation as critical regulator of hepatic alterations. Abundance of c-jun in NAFLD likely facilitates development and progression of NASH, and thus, c-jun appears as attractive prognostic and therapeutic target of NAFLD progression. 14-weeks old male C57BL/6N mice were fed with either regular diet or a newly designed NASH-inducing diet for 12 weeks. Hepatic gene expression levels were measured thereafter.
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2013-08-30 | GSE49541 | GEO
Project description:We report the effect of NAFLD on liver gene expression changes that could impact tetrachloroethhylene metabolism Methods: We fed male C57Bl/6J mice a base diet (BD), high fat (HFD), or methionine/choline/folate deficient high fat diet (MCD) for 8 weeks and then treated them with vehicle or tetrachloroethylene (PERC, 300 mg/kg ig). We only report "basal" differences herein (aka vehicle-treated). Results: We report that there were diet-specific differences in xenobiotic metabolizing genes, and that these genes may be responsible for NAFLD-induced disruption in PERC metabolism
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Project description:Kinase activity of cGMP-dependant, type II, protein kinase (PRKG2) is required for the proliferative to hypertrophic growth transition of growth plate chondrocytes during endochondral ossification. Loss of PRKG2 function in rodent and bovine models results in dwarfism. We compared growth plate cartilage gene expression profiles of PRKG2R678X/R678X, dwarf and PRKG2R678X/+, unaffected Angus cattle using microarray technology to discover pathways regulated by PRKG2. Calves used in this analysis were produced by the mating between a dwarf carrier sire and two dams- a mother (carrier) and daughter (dwarf) pair. Each dam produced three calves by embryo transfer, which were born in two calving groups. Growth plate cartilage was harvested from the tibia of each animal at approximately 215 days of age. Total RNA was extracted by a modified Trizol protocol. The bovine cDNA microarray (GEO Accession: GPL8813) was used for this analysis. Samples were labeled with Cy3 or Cy5 and hybridized by dye swapping the dwarf (4 dwarf animals- 2 per dam/calving group) and unaffected individuals (2 unaffected animals- 1 per dam/ calving group) such that each dwarf was compared to the unaffected full-sib produced in the same calving group. Each cDNA array was analyzed at three different PMT levels (PMT70,80 and 90), resulting in 12 total image files for statistical analysis. Dwarf PRKG2 R678X homozygous cattle were compared to unaffected, age matched samples. Samples were labeled with Cy3 or Cy5 and hybridized by dye swapping the dwarf (4 dwarf animals- 2 per dam/calving group) and unaffected individuals (2 unaffected animals- 1 per dam/ calving group) such that each dwarf was compared to the unaffected full-sib produced in the same calving group (i.e. unaffected samples had 2 technical replicates). Each cDNA array was analyzed at three different PMT levels (PMT70,80 and 90), resulting in 12 total image files for statistical analysis.
2011-08-24 | E-GEOD-31627 | biostudies-arrayexpress