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Conference Paper: Decreased adiponectin and antioxidant enzymes are associated with necroinflammatory changes and fibrosis in a rat model for non-alcoholic fatty liver disease (NAFLD)

TitleDecreased adiponectin and antioxidant enzymes are associated with necroinflammatory changes and fibrosis in a rat model for non-alcoholic fatty liver disease (NAFLD)
Authors
Issue Date2008
PublisherSpringer New York LLC. The Journal's web site is located at http://www.springer.com/west/home/medicine?SGWID=4-10054-70-173733513-0
Citation
The 4th Hong Kong-Shanghai International Liver Congress (ILC), Hong Kong, 12–15 June 2008. In Hepatology International, 2008, v. 2 n. S2, p. S151-S152, abstract no. PP-302 How to Cite?
AbstractNAFLD is a chronic liver disease characterized by fatty liver, necroinflammation and fibrosis. We fed a diet containing 30% fish oil to female Sprague-Dawley rats (180-200g), consumed ad libitum for 8 weeks (NAFLD; n = 8). Control animals (CF; n = 8) were fed with isocaloric rat chow. At killing, blood and liver samples were collected for serum alanine aminotransferase (ALT), histology and molecular analysis. Histological sample was evaluated for fatty liver, necrosis and inflammation. Collagen was estimated based on the degree of Sirius Red staining. RT-PCR was carried out for adiponectin, glutathione peroxidase (GPx), superoxide dismutase (Cu/Zn SOD), catalase (CAT), TGF-ȕ1, procollagen (Pro-col), tissue inhibitors of metalloproteinases (TIMP-1; TIMP-2) matrix metalloproteinase (MMP-2). Zymography was performed to determine the enzyme activity of MMP-2. Electrophoretic mobility shift assay was done for nuclear factor-kappa B (NF-țB) activity. NAFLD rats had significantly higher serum ALT, fatty liver, necrosis, inflammation and amount of collagen formation. The mRNAs of GPx and CAT were reduced in NAFLD rats but the Cu/Zn SOD level was not altered. Liver adiponectin was also significantly diminished in NAFLD rats. mRNA levels of TGF-ȕ1, Pro-col, TIMP-1, TIMP-2 and MMP-2 were also significantly upregulated in the NAFLD group when compared to CF rats. MMP-2 enzyme and NF-țB activity were also markedly increased in the NAFLD rats. Our study shows that fatty liver and necroinflammation are accompanied by reduction in the antioxidant enzymes (GPx and CAT) and adiponectin. Liver fibrosis, another important feature of NAFLD was accompanied by upregulation of profibrogenic mediators.
Persistent Identifierhttp://hdl.handle.net/10722/95504
ISSN
2021 Impact Factor: 9.029
2020 SCImago Journal Rankings: 1.304
PubMed Central ID

 

DC FieldValueLanguage
dc.contributor.authorHo, CTen_HK
dc.contributor.authorTipoe, GLen_HK
dc.contributor.authorLiong, ECen_HK
dc.contributor.authorLeung, TMen_HK
dc.contributor.authorLau, TYHen_HK
dc.contributor.authorFung, MLen_HK
dc.contributor.authorNanji, AAen_HK
dc.date.accessioned2010-09-25T16:04:22Z-
dc.date.available2010-09-25T16:04:22Z-
dc.date.issued2008en_HK
dc.identifier.citationThe 4th Hong Kong-Shanghai International Liver Congress (ILC), Hong Kong, 12–15 June 2008. In Hepatology International, 2008, v. 2 n. S2, p. S151-S152, abstract no. PP-302en_HK
dc.identifier.issn1936-0533en_HK
dc.identifier.urihttp://hdl.handle.net/10722/95504-
dc.description.abstractNAFLD is a chronic liver disease characterized by fatty liver, necroinflammation and fibrosis. We fed a diet containing 30% fish oil to female Sprague-Dawley rats (180-200g), consumed ad libitum for 8 weeks (NAFLD; n = 8). Control animals (CF; n = 8) were fed with isocaloric rat chow. At killing, blood and liver samples were collected for serum alanine aminotransferase (ALT), histology and molecular analysis. Histological sample was evaluated for fatty liver, necrosis and inflammation. Collagen was estimated based on the degree of Sirius Red staining. RT-PCR was carried out for adiponectin, glutathione peroxidase (GPx), superoxide dismutase (Cu/Zn SOD), catalase (CAT), TGF-ȕ1, procollagen (Pro-col), tissue inhibitors of metalloproteinases (TIMP-1; TIMP-2) matrix metalloproteinase (MMP-2). Zymography was performed to determine the enzyme activity of MMP-2. Electrophoretic mobility shift assay was done for nuclear factor-kappa B (NF-țB) activity. NAFLD rats had significantly higher serum ALT, fatty liver, necrosis, inflammation and amount of collagen formation. The mRNAs of GPx and CAT were reduced in NAFLD rats but the Cu/Zn SOD level was not altered. Liver adiponectin was also significantly diminished in NAFLD rats. mRNA levels of TGF-ȕ1, Pro-col, TIMP-1, TIMP-2 and MMP-2 were also significantly upregulated in the NAFLD group when compared to CF rats. MMP-2 enzyme and NF-țB activity were also markedly increased in the NAFLD rats. Our study shows that fatty liver and necroinflammation are accompanied by reduction in the antioxidant enzymes (GPx and CAT) and adiponectin. Liver fibrosis, another important feature of NAFLD was accompanied by upregulation of profibrogenic mediators.-
dc.languageengen_HK
dc.publisherSpringer New York LLC. The Journal's web site is located at http://www.springer.com/west/home/medicine?SGWID=4-10054-70-173733513-0en_HK
dc.relation.ispartofHepatology Internationalen_HK
dc.titleDecreased adiponectin and antioxidant enzymes are associated with necroinflammatory changes and fibrosis in a rat model for non-alcoholic fatty liver disease (NAFLD)en_HK
dc.typeConference_Paperen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1936-0533&volume=2&spage=S151&epage=S152&date=2008&atitle=Decreased+adiponectin+and+antioxidant+enzymes+are+associated+with+necroinflammatory+changes+and+fibrosis+in+a+rat+model+for+non-alcoholic+fatty+liver+disease+(NAFLD)en_HK
dc.identifier.emailTipoe, GL: tgeorge@hkucc.hku.hken_HK
dc.identifier.emailLiong, EC: eclionga@HKUCC.hku.hken_HK
dc.identifier.emailLeung, TM: leungtm@hkucc.hku.hken_HK
dc.identifier.emailFung, ML: fungml@hkucc.hku.hken_HK
dc.identifier.authorityTipoe, GL=rp00371en_HK
dc.identifier.authorityFung, ML=rp00433en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1007/s12072-008-9079-9-
dc.identifier.pmcidPMC2716912-
dc.identifier.hkuros145276en_HK
dc.identifier.hkuros153235-
dc.identifier.hkuros155361-
dc.identifier.volume2en_HK
dc.identifier.issue2 suppl.-
dc.identifier.spageS151, abstract no. PP-302en_HK
dc.identifier.epageS152en_HK
dc.identifier.issnl1936-0533-

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