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Article: Characterization of high-fat, diet-induced, non-alcoholic steatohepatitis with fibrosis in rats

TitleCharacterization of high-fat, diet-induced, non-alcoholic steatohepatitis with fibrosis in rats
Authors
KeywordsAnimal model
Fibrosis
Non-alcoholic steatohepatitis
Rat
Issue Date2010
PublisherSpringer New York LLC. The Journal's web site is located at http://springerlink.metapress.com/openurl.asp?genre=journal&issn=0163-2116
Citation
Digestive Diseases And Sciences, 2010, v. 55 n. 4, p. 931-940 How to Cite?
AbstractAn ideal animal model is necessary for a clear understanding of the etiology, pathogenesis, and mechanisms of human non-alcoholic steatohepatitis (NASH) and for facilitating the design of effective therapy for this condition. We aimed to establish a rat model of NASH with fibrosis by using a high-fat diet (HFD). Male Sprague-Dawley (SD) rats were fed a HFD consisting of 88 g normal diet, 10 g lard oil, and 2 g cholesterol. Control rats were fed normal diet. Rats were killed at 4, 8, 12, 16, 24, 36, and 48 weeks after HFD exposure. Body weight, liver weight, and epididymal fat weight were measured. Serum levels of fasting glucose, triglyceride, cholesterol, alanine aminotransferase (ALT), free fatty acids (FFA), insulin, and tumor necrosis factor-alpha (TNF-α) were determined. Hepatic histology was examined by H&E stain. Hepatic fibrosis was assessed by VG stain and immunohistochemical staining for transforming growth factor beta 1 (TGF-β1), and alpha-smooth-muscle actin (α-SMA). The liver weight and liver index increased from week 4, when hepatic steatosis was also observed. By week 8, the body weight and epididymal fat weight started increasing, which was associated with increased serum levels of FFA, cholesterol, and TNF-α, as well as development of simple fatty liver. The serum ALT level increased from week 12. Steatohepatitis occurred from weeks 12 through 48. Apparent hepatic perisinosodial fibrosis did not occur until week 24, and progressed from week 36 to 48 with insulin resistance. Therefore, this novel model may be potentially useful in NASH study. © 2009 Springer Science+Business Media, LLC.
Persistent Identifierhttp://hdl.handle.net/10722/59286
ISSN
2015 Impact Factor: 2.516
2015 SCImago Journal Rankings: 0.995
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorXu, ZJen_HK
dc.contributor.authorFan, JGen_HK
dc.contributor.authorDing, XDen_HK
dc.contributor.authorQiao, Len_HK
dc.contributor.authorWang, GLen_HK
dc.date.accessioned2010-05-31T03:47:01Z-
dc.date.available2010-05-31T03:47:01Z-
dc.date.issued2010en_HK
dc.identifier.citationDigestive Diseases And Sciences, 2010, v. 55 n. 4, p. 931-940en_HK
dc.identifier.issn0163-2116en_HK
dc.identifier.urihttp://hdl.handle.net/10722/59286-
dc.description.abstractAn ideal animal model is necessary for a clear understanding of the etiology, pathogenesis, and mechanisms of human non-alcoholic steatohepatitis (NASH) and for facilitating the design of effective therapy for this condition. We aimed to establish a rat model of NASH with fibrosis by using a high-fat diet (HFD). Male Sprague-Dawley (SD) rats were fed a HFD consisting of 88 g normal diet, 10 g lard oil, and 2 g cholesterol. Control rats were fed normal diet. Rats were killed at 4, 8, 12, 16, 24, 36, and 48 weeks after HFD exposure. Body weight, liver weight, and epididymal fat weight were measured. Serum levels of fasting glucose, triglyceride, cholesterol, alanine aminotransferase (ALT), free fatty acids (FFA), insulin, and tumor necrosis factor-alpha (TNF-α) were determined. Hepatic histology was examined by H&E stain. Hepatic fibrosis was assessed by VG stain and immunohistochemical staining for transforming growth factor beta 1 (TGF-β1), and alpha-smooth-muscle actin (α-SMA). The liver weight and liver index increased from week 4, when hepatic steatosis was also observed. By week 8, the body weight and epididymal fat weight started increasing, which was associated with increased serum levels of FFA, cholesterol, and TNF-α, as well as development of simple fatty liver. The serum ALT level increased from week 12. Steatohepatitis occurred from weeks 12 through 48. Apparent hepatic perisinosodial fibrosis did not occur until week 24, and progressed from week 36 to 48 with insulin resistance. Therefore, this novel model may be potentially useful in NASH study. © 2009 Springer Science+Business Media, LLC.en_HK
dc.languageengen_HK
dc.publisherSpringer New York LLC. The Journal's web site is located at http://springerlink.metapress.com/openurl.asp?genre=journal&issn=0163-2116en_HK
dc.relation.ispartofDigestive Diseases and Sciencesen_HK
dc.rightsThe original publication is available at www.springerlink.com-
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subjectAnimal modelen_HK
dc.subjectFibrosisen_HK
dc.subjectNon-alcoholic steatohepatitisen_HK
dc.subjectRaten_HK
dc.subject.meshActins - metabolism-
dc.subject.meshDietary Fats - pharmacology-
dc.subject.meshDisease Models, Animal-
dc.subject.meshFatty Liver - pathology-
dc.subject.meshLiver Cirrhosis, Experimental - immunology - pathology-
dc.titleCharacterization of high-fat, diet-induced, non-alcoholic steatohepatitis with fibrosis in ratsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0163-2116&volume=55&issue=4&spage=931&epage=940&date=2010&atitle=Characterization+of+high-fat,+diet-induced,+non-alcoholic+steatohepatitis+with+fibrosis+in+rats-
dc.identifier.emailQiao, L: lq8688@hotmail.comen_HK
dc.identifier.authorityQiao, L=rp00513en_HK
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1007/s10620-009-0815-3en_HK
dc.identifier.pmid19459046-
dc.identifier.pmcidPMC2946554-
dc.identifier.scopuseid_2-s2.0-77950355485en_HK
dc.identifier.hkuros155751en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77950355485&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume55en_HK
dc.identifier.issue4en_HK
dc.identifier.spage931en_HK
dc.identifier.epage940en_HK
dc.identifier.eissn1573-2568en_HK
dc.identifier.isiWOS:000276153900009-
dc.publisher.placeUnited Statesen_HK
dc.description.otherSpringer Open Choice, 01 Dec 2010-
dc.identifier.scopusauthoridXu, ZJ=7405428888en_HK
dc.identifier.scopusauthoridFan, JG=7402794878en_HK
dc.identifier.scopusauthoridDing, XD=7401929643en_HK
dc.identifier.scopusauthoridQiao, L=7202151719en_HK
dc.identifier.scopusauthoridWang, GL=24342481800en_HK
dc.identifier.citeulike4626930-

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