Unknown,Transcriptomics,Genomics,Proteomics

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Rab46 and the liver

ABSTRACT: Non-alcoholic fatty liver disease (NAFLD), a chronic liver condition characterised by excessive fat in the liver, is associated with insulin resistance (as in type II diabetes), obesity and lipidaemia. The progression of NAFLD to NASH is multifactorial, however, the underlying mechanisms are not well understood and whilst a population of patients develop NASH some, with the same co-morbidities and risk factors, just have a fatty liver. Recently a pilot GWAS in patients with NAFLD looked at genetic variants significantly associated with hepatic histology. They identified rs887304 on chromosome 12 in EFCAB4B to be associated with lobular inflammation. It is important therefore to understand the contribution of CRACR2A and Rab46 to liver function. Here we utilized an Efcab4b global knockout mouse to explore the gene expression in liver.

INSTRUMENT(S): Illumina HiSeq 4000, Illumina

ORGANISM(S): Mus musculus

SUBMITTER: Chew Weng Cheng

PROVIDER: E-MTAB-13110 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:The pathological progression of nonalcoholic fatty liver disease (NAFLD) is driven by multiple factors, and nonalcoholic steatohepatitis (NASH) represents its progressive form. In our previous studies, we found that bicyclol had beneficial effects on NAFLD/NASH. Here we aim to investigate the underlying molecular mechanisms of the bicyclol effect on NAFLD/NASH induced by high-fat diet (HFD) feeding. A mice model of NAFLD/NASH induced by HFD-feeding for 8 weeks was used. As a pretreatment, bicyclol (200 mg/kg) was given to mice by oral gavage twice daily. Hematoxylin and eosin (H&E) stains were processed to evaluate hepatic steatosis, and hepatic fibrous hyperplasia was assessed by Masson staining. Biochemistry analyses were used to measure serum aminotransferase, serum lipids, and lipids in liver tissues. Proteomics and bioinformatics analyses were performed to identify the signaling pathways and target proteins. The real-time RT-PCR and Western blot analyses were performed to verify the proteomics data. As a result, bicyclol had a markedly protective effect against NAFLD/NASH by suppressing the increase of serum aminotransferase, hepatic lipid accumulation and alleviating histopathological changes in liver tissues. Proteomics analyses showed that bicyclol remarkably restored major pathways related to immunological responses and metabolic processes altered by HFD feeding. Consistent with our previous results, bicyclol significantly inhibited inflammation and oxidative stress pathway related indexes (SAA1, GSTM1 and RDH11). Furthermore, the beneficial effects of bicyclol were closely associated with the signaling pathways of bile acid metabolism (NPC1, SLCOLA4 and UGT1A1), cytochrome P450-mediated metabolism (CYP2C54, CYP2C70 and CYP3A25), biological processes such as metal ion metabolism (Ceruloplasmin and Metallothionein-1), angiogenesis (ALDH1A1) and immunological responses (IFI204 and IFIT3). These findings suggested that bicyclol is a potential preventive agent for NAFLD/NASH by targeting multiple mechanisms in future clinical investigations.

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Rab46 and the liver

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