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Article: Lipoprotein lipase activator ameliorates the severity of dietary steatohepatitis
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TitleLipoprotein lipase activator ameliorates the severity of dietary steatohepatitis
 
AuthorsYu, J1
Chu, ESH1
Hui, AY1
Cheung, KF1
Chan, HLY1
Leung, WK1
Farrell, GC2
Sung, JJY1
 
KeywordsSpecies Index: Mus
 
Issue Date2007
 
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/wps/find/journaldescription.cws_home/622790/description
 
CitationBiochemical And Biophysical Research Communications, 2007, v. 356 n. 1, p. 53-59 [How to Cite?]
DOI: http://dx.doi.org/10.1016/j.bbrc.2007.02.129
 
AbstractDietary model of steatohepatitis was established by feeding mice a methionine choline deficient (MCD) diet. Mice on MCD or control diet for 3 weeks were treated with or without NO-1886, a newly synthetic lipoprotein lipase (LPL) activator. In a separate experiment, NO-1886 was given after pre-treatment with 3 weeks of MCD diet. NO-1886 significantly reduced MCD-induced inflammation by repressing levels of hepatic lipid peroxides and pro-inflammatory tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and cyclooxygenase-2 (COX-2). In addition, NO-1886 dampened hepatic steatosis via accelerating fatty acid oxidation caused by enhanced expression of PPARα, cytochrome P450-10 (Cyp4a10), and Acyl-CoA oxidase (ACO). It failed to regulate genes of fatty acid uptake and synthesis pathways. In conclusion, NO-1886 ameliorated and induced regression of experimental steatohepatitis via increasing endogenous LPL activation resulting in suppression on pro-inflammatory factors and reduction of hepatic fatty acids. These findings indicate that NO-1886 is a potential therapeutic agent for steatohepatitis. © 2007 Elsevier Inc. All rights reserved.
 
ISSN0006-291X
2013 Impact Factor: 2.281
 
DOIhttp://dx.doi.org/10.1016/j.bbrc.2007.02.129
 
ISI Accession Number IDWOS:000245419300009
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorYu, J
 
dc.contributor.authorChu, ESH
 
dc.contributor.authorHui, AY
 
dc.contributor.authorCheung, KF
 
dc.contributor.authorChan, HLY
 
dc.contributor.authorLeung, WK
 
dc.contributor.authorFarrell, GC
 
dc.contributor.authorSung, JJY
 
dc.date.accessioned2011-04-04T07:57:26Z
 
dc.date.available2011-04-04T07:57:26Z
 
dc.date.issued2007
 
dc.description.abstractDietary model of steatohepatitis was established by feeding mice a methionine choline deficient (MCD) diet. Mice on MCD or control diet for 3 weeks were treated with or without NO-1886, a newly synthetic lipoprotein lipase (LPL) activator. In a separate experiment, NO-1886 was given after pre-treatment with 3 weeks of MCD diet. NO-1886 significantly reduced MCD-induced inflammation by repressing levels of hepatic lipid peroxides and pro-inflammatory tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and cyclooxygenase-2 (COX-2). In addition, NO-1886 dampened hepatic steatosis via accelerating fatty acid oxidation caused by enhanced expression of PPARα, cytochrome P450-10 (Cyp4a10), and Acyl-CoA oxidase (ACO). It failed to regulate genes of fatty acid uptake and synthesis pathways. In conclusion, NO-1886 ameliorated and induced regression of experimental steatohepatitis via increasing endogenous LPL activation resulting in suppression on pro-inflammatory factors and reduction of hepatic fatty acids. These findings indicate that NO-1886 is a potential therapeutic agent for steatohepatitis. © 2007 Elsevier Inc. All rights reserved.
 
dc.description.naturelink_to_subscribed_fulltext
 
dc.identifier.citationBiochemical And Biophysical Research Communications, 2007, v. 356 n. 1, p. 53-59 [How to Cite?]
DOI: http://dx.doi.org/10.1016/j.bbrc.2007.02.129
 
dc.identifier.doihttp://dx.doi.org/10.1016/j.bbrc.2007.02.129
 
dc.identifier.eissn1090-2104
 
dc.identifier.epage59
 
dc.identifier.isiWOS:000245419300009
 
dc.identifier.issn0006-291X
2013 Impact Factor: 2.281
 
dc.identifier.issue1
 
dc.identifier.pmid17350593
 
dc.identifier.scopuseid_2-s2.0-33947172627
 
dc.identifier.spage53
 
dc.identifier.urihttp://hdl.handle.net/10722/132852
 
dc.identifier.volume356
 
dc.languageeng
 
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/wps/find/journaldescription.cws_home/622790/description
 
dc.publisher.placeUnited States
 
dc.relation.ispartofBiochemical and Biophysical Research Communications
 
dc.relation.referencesReferences in Scopus
 
dc.subject.meshAnimals
 
dc.subject.meshBenzamides - administration & dosage - pharmacology
 
dc.subject.meshCholesterol - blood
 
dc.subject.meshCholine Deficiency
 
dc.subject.meshCyclooxygenase 2 - genetics - metabolism
 
dc.subject.meshDiet - adverse effects
 
dc.subject.meshEnzyme Activation - drug effects
 
dc.subject.meshFatty Liver - blood - etiology - prevention & control
 
dc.subject.meshGene Expression - drug effects
 
dc.subject.meshHypolipidemic Agents - administration & dosage - pharmacology
 
dc.subject.meshIntercellular Adhesion Molecule-1 - genetics - metabolism
 
dc.subject.meshInterleukin-6 - genetics - metabolism
 
dc.subject.meshLipogenesis - genetics
 
dc.subject.meshLipoprotein Lipase - genetics - metabolism
 
dc.subject.meshLipoproteins, HDL - blood
 
dc.subject.meshLiver - drug effects - metabolism - pathology
 
dc.subject.meshMale
 
dc.subject.meshMethionine - deficiency
 
dc.subject.meshMice
 
dc.subject.meshMice, Inbred C57BL
 
dc.subject.meshOrganophosphorus Compounds - administration & dosage - pharmacology
 
dc.subject.meshPPAR gamma - genetics - metabolism
 
dc.subject.meshRNA, Messenger - genetics - metabolism
 
dc.subject.meshThiobarbituric Acid Reactive Substances - metabolism
 
dc.subject.meshTumor Necrosis Factor-alpha - genetics - metabolism
 
dc.subjectSpecies Index: Mus
 
dc.titleLipoprotein lipase activator ameliorates the severity of dietary steatohepatitis
 
dc.typeArticle
 
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<contributor.author>Chan, HLY</contributor.author>
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Author Affiliations
  1. Prince of Wales Hospital Hong Kong
  2. Australian National University