dc.contributorUniversidade Estadual Paulista (Unesp)
dc.date.accessioned2014-05-20T15:24:50Z
dc.date.available2014-05-20T15:24:50Z
dc.date.created2014-05-20T15:24:50Z
dc.date.issued1993-01-01
dc.identifierBrazilian Journal of Medical and Biological Research. São Paulo: Associação Bras Divulg Cientifica, v. 26, n. 1, p. 31-36, 1993.
dc.identifier0100-879X
dc.identifierhttp://hdl.handle.net/11449/35370
dc.identifierWOS:A1993KP41900003
dc.description.abstractThe ability of high dietary carbohydrate to induce acute pancreatitis was investigated in groups of 16,2 1-day and 15-month old rats fed different carbohydrate diets for 30 days. Significantly increased levels of serum amylase (2-fold), phospholipids (50%),phosphorus (2-fold), and lipoperoxides (8-fold) were observed in 15-month old rats fed a high-carbohydrate diet, compared to rats fed a diet with normal carbohydrate levels, indicating peroxidation of membrane lipids which caused final cell death and pancreatic lesion. Serum Cu-Zn superoxide dismutase activity was not altered. Daily administration of bovine Cu-Zn superoxide dismutase conjugated with polyediylene glycol prevented the serum level alterations and pancreatic lesions, indicating that the superoxide radical has a role in dietary carbohydrate-induced acute pancreatitis. No biochemical changes were observed in rats in which treatment was initiated on the 21st day of life indicating that this is an age-related lesion.
dc.languageeng
dc.publisherAssociação Brasileira de Divulgação Científica (ABRADIC)
dc.relationBrazilian Journal of Medical and Biological Research
dc.relation1.492
dc.rightsAcesso restrito
dc.sourceWeb of Science
dc.subjectCARBOHYDRATE
dc.subjectPANCREATIC LESION
dc.subjectSUPEROXIDE DISMUTASE
dc.titleHIGH DIETARY CARBOHYDRATE AND PANCREATIC LESION
dc.typeArtículos de revistas


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