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dc.contributor.authorArranz Sanz, Eduardo 
dc.date.accessioned2014-02-06T16:48:49Z
dc.date.available2014-02-06T16:48:49Z
dc.date.issued2009
dc.identifier.citationGut, vol.000, n.000. p.1-2es
dc.identifier.urihttp://uvadoc.uva.es/handle/10324/4240
dc.descriptionProducción Científicaes
dc.description.abstractProlyl-endopeptidase supplementation has been proposed to favour gliadin degradation as an alternative treatment for coeliac disease (CD), although the real usefulness of this therapy in vivo is still under discussion. 1 However, our data point to alternative treatments aiming to modify the intestinal microbiota in patients with CD by the use of probiotics and/or prebiotics. We propose that the induction of gliadin proteolysis in the human gut might not be the solution but the origin of CD.es
dc.format.mimetypeapplication/pdfes
dc.language.isospaes
dc.publisherInstituto de Biología y Genética Molecula (IBGM)es
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/
dc.subjectEnfermedad celíacaes
dc.titleIs it true that coeliacs do not digest gliadin?. Degradation pattern of gliadin in coeliac disease small intestinal mucosaes
dc.typeinfo:eu-repo/semantics/articlees
dc.identifier.doi10.1136/gut 2008-167296es
dc.identifier.publicationfirstpage1es
dc.identifier.publicationissue0es
dc.identifier.publicationlastpage2es
dc.identifier.publicationtitleGutes
dc.identifier.publicationvolume0es
dc.peerreviewedSIes
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 International


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