Analysis Tools
homeostasis/metabolism
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• male mice fed either a standard control (SC) diet or a choline-deficient, L-amino acid-defined, high-fat diet (CDAHFD) for 8 weeks show hepatic bile acid (BA) pools that are more conducive to liver fibrosis development, with significantly increased hydrophobic 12alpha-OH BAs [cholic acids (CAs) and deoxycholic acids (DCAs)] and decreased hydrophilic non-12alpha-OH BAs [muricholic acids (MCAs), hyodeoxycholic acids (HDCAs) and ursodeoxycholic acids (UDCAs)]
• UDCA (hydrophilic non-12alpha-OH BA) is significantly decreased by CDAHFD feeding, such that CDAHFD-fed males show a further reduction in UDCA content relative to SC-fed males and CDAHFD-fed wild-type controls
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• male mice fed a CDAHFD for 8 weeks show more severe liver fibrosis, an increased number of hepatic alpha-SMA-positive cells, and higher mRNA expression levels of hepatic fibrosis factors (Acta2, Col1a1, and Tgfb1) than CDAHFD-fed wild-type controls
• however, CDAHFD-fed males show no differences in the severity of liver steatosis and inflammation, as indicated by similar gross liver morphology, liver weight/body weight index, serum transaminase levels, liver histology, and expression of hepatic inflammatory factors relative to CDAHFD-fed controls
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liver/biliary system
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• CDAHFD-fed males show more severe liver fibrosis than CDAHFD-fed wild-type controls, as determined by Masson and Sirius red staining
• profibrotic effect might be attributed to inhibition of BA alternative synthesis pathway
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• males fed either a SC diet or a CDAHFD show a significant decrease in hepatic mRNA and protein levels of Cyp27a1 (a key enzyme in the alternative pathway of bile acid synthesis) relative to diet-matched controls
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