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Screening of Genes Related to Glucose and Lipid Metabolism in Non-alcoholic Fatty Liver Disease by Gene Microarray

ABSTRACT: We used gene expression microarray to explore the correlation between gene expression profiles and find out the target genes related to lipid and glucose metabolism in NAFLD. A rat model of NAFLD was established by feeding male rats with high-fat diet and Agilent DNA microarray was used to detect gene expression profiles of liver tissues. We explored differentially expressed genes and intersection of them by using Gene ontology (GO) and Pathway analyses. Then, target genes were verified by Real-time polymerase chain reaction (RT-PCR). There were 932 genes, including 783 up-regulated and 149 down-regulated, differed in expression compared to those of control rats. The up-regulated genes were involved in biosynthesis, cell development, cell differentiation and down-regulated genes mainly contributed to biological metabolic process and stress reaction. We identified genes involved in insulin signaling pathway, Notch signaling pathway, adipocytokin and linoleic acid metabolism to be closely related to liver fat content and insulin resistance. Among them, genes which supposed to connect glucose and lipid metabolism were screened (IGFBP7, Notch1, HMGCR and ACACB) and then validated by real-time PCR. These data provide innovative information on the whole genome expression profile due to high-fat diet feeding and bring important insights into the mechanism of NAFLD.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE118892 | GEO | 2021/08/10

REPOSITORIES: GEO

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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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Screening of Genes Related to Glucose and Lipid Metabolism in Non-alcoholic Fatty Liver Disease by Gene Microarray

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