Please use this identifier to cite or link to this item: https://olympias.lib.uoi.gr/jspui/handle/123456789/24658
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dc.contributor.authorKalamidas, S. A.en
dc.contributor.authorKondomerkos, D. J.en
dc.date.accessioned2015-11-24T19:42:33Z-
dc.date.available2015-11-24T19:42:33Z-
dc.identifier.issn1097-0029-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/24658-
dc.rightsDefault Licence-
dc.subject3-O-Methylglucose/administration & dosage/pharmacologyen
dc.subjectAnimalsen
dc.subjectAnimals, Newbornen
dc.subjectAutophagy/*drug effectsen
dc.subjectBlood Glucoseen
dc.subjectDeoxyglucose/administration & dosage/pharmacologyen
dc.subjectGlucan 1,4-alpha-Glucosidase/metabolismen
dc.subject*Glucose/administration & dosage/analogs & derivatives/metabolism/pharmacologyen
dc.subjectGlycogen/chemistry/*metabolismen
dc.subject*Hepatocytes/drug effects/metabolismen
dc.subjectHistocytochemistryen
dc.subjectLiver/cytology/enzymology/metabolismen
dc.subjectMicroscopyen
dc.subjectPhotomicrographyen
dc.subjectPropranolol/administration & dosage/pharmacologyen
dc.subjectRatsen
dc.subjectRats, Wistaren
dc.subjectVacuoles/chemistry/metabolismen
dc.titleThe administration of nonmetabolizable glucose analogues fails to suppress the development of glycogen autophagy in newborn rat hepatocytesen
heal.typejournalArticle-
heal.type.enJournal articleen
heal.type.elΆρθρο Περιοδικούel
heal.identifier.primary10.1002/jemt.20825-
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/20146348-
heal.identifier.secondaryhttp://onlinelibrary.wiley.com/store/10.1002/jemt.20825/asset/20825_ftp.pdf?v=1&t=h0ko71mg&s=018ec9cdd3869a195bf68f4a0cc62b23766c7c09-
heal.languageen-
heal.accesscampus-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.publicationDate2010-
heal.abstractThe effects of parenteral administration of glucose, 3-methylglucose (3MG), or 2-deoxyglucose (2DG) on the glycogen autophagy were studied in the newborn rat liver using electron microscopy and biochemical methods. The administration of glucose resulted in hyperglycemia and prevented the mobilization of hepatocytic glycogen. It also prevented the development of autophagic vacuoles in general and inhibited the glycogen-degrading activity of acid alpha-1,4-glucosidase. The nonphosphorylated and not further metabolized glucose analog 3MG also produced hyperglycemia, but increased acid glucosidase. Pretreating the newborns with the beta-adrenergic blocker propranolol inhibited the effects of 3MG. The phosphorylated but not fully metabolized glucose analog 2DG produced similar effects. The administration of xylitol to the newborns already treated with 2DG, suppressed acid glucosidase. The results of this and our previous studies suggest that glucose must be metabolized beyond its phosphorylation step to inhibit acid glucosidase activity.en
heal.journalNameMicrosc Res Techen
heal.journalTypepeer-reviewed-
heal.fullTextAvailabilityTRUE-
Appears in Collections:Άρθρα σε επιστημονικά περιοδικά ( Ανοικτά) - ΙΑΤ

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