Long-term ethanol consumption promotes hepatic tumorigenesis but impairs normal hepatocyte proliferation in rats

dc.contributorUniversidade Estadual Paulista (UNESP)
dc.creatorChavez, Pollyanna R. G.
dc.creatorLian, Fuzhi
dc.creatorChung, Jayong
dc.creatorLiu, Chun
dc.creatorPaiva, Sergio Alberto Rupp de
dc.creatorSeitz, Helmut K.
dc.creatorWang, Xiang-Dong
dc.date2014-05-27T11:25:54Z
dc.date2016-10-25T18:34:01Z
dc.date2014-05-27T11:25:54Z
dc.date2016-10-25T18:34:01Z
dc.date2011-06-01
dc.date.accessioned2017-04-06T01:50:50Z
dc.date.available2017-04-06T01:50:50Z
dc.identifierJournal of Nutrition, v. 141, n. 6, p. 1049-1055, 2011.
dc.identifier0022-3166
dc.identifier1541-6100
dc.identifierhttp://hdl.handle.net/11449/72473
dc.identifierhttp://acervodigital.unesp.br/handle/11449/72473
dc.identifier10.3945/jn.110.136531
dc.identifier2-s2.0-79958189574
dc.identifierhttp://dx.doi.org/10.3945/jn.110.136531
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/893341
dc.descriptionChronic and excessive alcohol consumption has been related to an increased risk of several cancers, including that of the liver; however, studies in animal models have yet to conclusively determine whether ethanol acts as a tumor promoter in hepatic tumorigenesis. We examined whether prolonged alcohol consumption could act as a hepatic tumor promoter after initiation by diethylnitrosamine (DEN) in a rat model. Male Sprague-Dawley rats were injected with 20 mg DEN/kg body weight 1 wk before introduction of either an ethanol liquid diet or an isoenergic control liquid diet. Hepatic pathological lesions, hepatocyte proliferation, apoptosis, PPARα and PPARγ, and plasma insulin-like growth factor 1 (IGF-1) levels were assessed after 6 and 10 mo. Mean body and liver weights, plasma IGF-1 concentration, hepatic expressions of proliferating cellular nuclear antigen and Ki-67, and cyclin D1 in ethanol-fed rats were all significantly lower after 10 mo of treatment compared with control rats. In addition, levels of hepatic PPARγ protein, not PPARα, were significantly higher in the ethanol-fed rats after prolonged treatment. Although ethanol feeding also resulted in significantly fewer altered hepatic foci, hepatocellular adenoma was detected in ethanol-fed rats at 10 mo, but not in control rats given the same dose of DEN. Together, these results indicate that chronic, excessive ethanol consumption impairs normal hepatocyte proliferation, which is associated with reduced IGF-1 levels, but promotes hepatic carcinogenesis. © 2011 American Society for Nutrition.
dc.languageeng
dc.relationJournal of Nutrition
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectalcohol
dc.subjectcyclin D1
dc.subjectcycline
dc.subjectdiethylnitrosamine
dc.subjectKi 67 antigen
dc.subjectperoxisome proliferator activated receptor alpha
dc.subjectperoxisome proliferator activated receptor gamma
dc.subjectsomatomedin C
dc.subjectalcohol consumption
dc.subjectanimal cell
dc.subjectanimal experiment
dc.subjectanimal tissue
dc.subjectantineoplastic activity
dc.subjectapoptosis
dc.subjectblood sampling
dc.subjectbody weight
dc.subjectcell proliferation
dc.subjectcontrolled study
dc.subjectdiet supplementation
dc.subjectdrug efficacy
dc.subjecthistopathology
dc.subjectliver
dc.subjectliver carcinogenesis
dc.subjectliver cell
dc.subjectliver weight
dc.subjectmale
dc.subjectnonhuman
dc.subjectpromoter region
dc.subjectprotein blood level
dc.subjectprotein expression
dc.subjectrat
dc.subjectAlcoholism
dc.subjectAnimals
dc.subjectApoptosis
dc.subjectCarcinogens
dc.subjectCell Proliferation
dc.subjectDiethylnitrosamine
dc.subjectEthanol
dc.subjectHepatocytes
dc.subjectInsulin-Like Growth Factor I
dc.subjectKi-67 Antigen
dc.subjectLiver Neoplasms, Experimental
dc.subjectMale
dc.subjectPPAR alpha
dc.subjectPPAR gamma
dc.subjectProliferating Cell Nuclear Antigen
dc.subjectRats
dc.subjectRats, Sprague-Dawley
dc.subjectAnimalia
dc.subjectRattus
dc.titleLong-term ethanol consumption promotes hepatic tumorigenesis but impairs normal hepatocyte proliferation in rats
dc.typeOtro


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