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dc.contributor.authorSolà, Anna M.-
dc.contributor.authorRoselló-Catafau, Joan-
dc.contributor.authorGelpí, Emili-
dc.contributor.authorHotter, Georgina-
dc.date.accessioned2008-02-18T18:19:44Z-
dc.date.available2008-02-18T18:19:44Z-
dc.date.issued2001-02-
dc.identifier.citationGut. 2001 February; 48(2): 168–175.en_US
dc.identifier.citationhttp://dx.doi.org/10.1136/gut.48.2.168en_US
dc.identifier.issn0017-5749-
dc.identifier.urihttp://hdl.handle.net/10261/2972-
dc.description.abstract[BACKGROUND AND AIMS] Inhibition of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) by nitric oxide (NO) in intestinal preconditioning could modify the rate of formation of glycolytic intermediates. Fructose-1,6-biphosphate (F16BP) is a glycolytic intermediate that protects tissue from ischaemia/reperfusion injury. We evaluated if F16BP may be endogenously accumulated as a consequence of GAPDH inhibition by NO during intestinal preconditioning in rats.en_US
dc.description.abstract[METHODS] We assessed: (1) effect of preconditioning on F16BP content; (2) effect of NO on GAPDH activity before and during sustained ischaemia; and (3) protective effect of F16BP in control, ischaemic, and preconditioned animals with or without administration of N-nitro-L-arginine methyl ester (L-NAME), NO donor, or F16BP.en_US
dc.description.abstract[RESULTS] Preconditioned rats showed a significant transient decrease in GAPDH activity and also maintained basal F16BP levels longer than ischaemic rats. L-NAME administration to preconditioned rats reversed these effects. F16BP administration to ischaemic rats decreased protein release in the perfusate. Administration of F16BP to L-NAME treated rats attenuated the harmful effect of L-NAME.en_US
dc.description.abstract[CONCLUSIONS] Our study indicates that F16BP may be endogenously accumulated in preconditioned rats as a consequence of inhibition of GAPDH by NO, and this may contribute to the protection observed in intestinal preconditioning.en_US
dc.description.sponsorshipThis work was supported by grant FIS 98/002901. A Sola was supported by a grant from Institut d’Investigacions Biomèdiques August Pi I Sunyer.en_US
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dc.format.mimetypeapplication/pdf-
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dc.language.isoengen_US
dc.publisherBMJ Publishing Groupen_US
dc.rightsopenAccessen_US
dc.subjectFructose-1,6-biphosphateen_US
dc.subjectGlyceraldehyde- 3-phosphate dehydrogenaseen_US
dc.subjectIntestinal preconditioningen_US
dc.subjectIschaemia/reperfusion injuryen_US
dc.subjectNitric Oxideen_US
dc.titleFructose-1,6-biphosphate in rat intestinal preconditioning: involvement of nitric oxideen_US
dc.typeartículoen_US
dc.identifier.doi10.1136/gut.48.2.168-
dc.description.peerreviewedPeer revieweden_US
dc.relation.publisherversionhttp://dx.doi.org/10.1136/gut.48.2.168-
dc.identifier.pmid11156636-
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fructose.pdfText file151,04 kBAdobe PDFThumbnail
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fructose_f1.jpgFigure 1.- Intestinal fructose-1,6-biphosphate (F16BP) levels during the different ischaemic periods (0, 2, 30, or 90 minutes) in the control.73,74 kBJPEGThumbnail
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fructose_f2.jpgFigure 2.- Intestinal glucose levels during the different ischaemic periods (0, 2, 30, or 90 minutes) in the control.47,05 kBJPEGThumbnail
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fructose_f3.jpgFigure 3.- GAPDH activity (U/mg protein) in the intestine during the different ischaemic periods (0, 2, 30, or 90 minutes) in the control.73,04 kBJPEGThumbnail
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fructose_f4.jpgFigure 4.- Nitrate and nitrite tissue production in the intestine in the following groups: control, control with previous administration of L-NAME (C+NAME), preconditioning.45,75 kBJPEGThumbnail
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fructose_f5.jpgFigure 5.- Profiles of protein release during the different ischaemic (0, 2, 30, and 90 minutes) and reperfusion.53,72 kBJPEGThumbnail
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fructose_f6.jpgFigure 6.- Intestinal fructose-1,6-biphosphate (F16BP) levels incorporated in the intestine.19,54 kBJPEGThumbnail
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