Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/20686
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dc.contributor.authorChoy, Suet-Wan-
dc.contributor.authorFraser, Scott A-
dc.contributor.authorKaterelos, Marina-
dc.contributor.authorGalic, Sandra-
dc.contributor.authorKemp, Bruce E-
dc.contributor.authorMount, Peter F-
dc.contributor.authorPower, David A-
dc.date2019-04-
dc.date.accessioned2019-04-30T23:55:25Z-
dc.date.available2019-04-30T23:55:25Z-
dc.date.issued2019-04-26-
dc.identifier.citationInternational Journal of Experimental Pathologyy 2019en_US
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/20686-
dc.description.abstractActivation of the heterotrimeric energy-sensing kinase AMP-activated protein kinase (AMPK) has been reported to improve experimental diabetic kidney disease. We examined the effect of type 1 diabetes in wild-type (WT) mice and mice lacking the β1 subunit of AMPK (AMPK β1-/- mice), which have reduced AMPK activity in kidneys and other organs. Diabetes was induced using streptozotocin (STZ) and the animals followed up for 4 weeks. Hyperglycaemia was more severe in diabetic AMPK β1-/- mice, despite the absence of any difference in serum levels of insulin, adiponectin and leptin. There was no change in AMPK activity in the kidneys of diabetic WT mice by AMPK activity assay, or phosphorylation of either the αT172 activation site on the α catalytic subunit of AMPK or the AMPK-specific phosphosite S79 on acetyl CoA carboxylase 1 (ACC1). Phosphorylation of the inhibitory αS485 site on the α subunit of AMPK was significantly increased in the WT diabetic mice compared to non-diabetic controls. Despite increased plasma glucose levels in the diabetic AMPK β1-/- mice, there were fewer myofibroblasts in the kidneys compared to diabetic WT mice, as evidenced by reduced α-smooth muscle actin (α-SMA) protein by Western blot, mRNA by qRT-PCR and fewer α-SMA-positive cells by immunohistochemical staining. Albuminuria was also reduced in the AMPK β1-/- mice. In contrast to previous studies, therefore, myofibroblasts were reduced in the kidneys of AMPK β1-/- diabetic mice compared to diabetic WT mice, despite increased circulating glucose, suggesting that AMPK can worsen renal fibrosis in type 1 diabetes.en_US
dc.language.isoeng-
dc.subjectAMPKen_US
dc.subjectdiabetesen_US
dc.subjectfibrosisen_US
dc.subjectmyofibroblasten_US
dc.titleAbsence of the β1 subunit of AMP-activated protein kinase reduces myofibroblast infiltration of the kidneys in early diabetes.en_US
dc.typeJournal Articleen_US
dc.identifier.journaltitleInternational Journal of Experimental Pathologyen_US
dc.identifier.affiliationMary MacKillop Institute for Health Research, Australian Catholic University, Fitzroy, Victoria, Australiaen_US
dc.identifier.affiliationDepartment of Nephrology, University of Melbourne, Heidelberg, Victoria, Australiaen_US
dc.identifier.affiliationDepartment of Medicine, University of Melbourne, St. Vincent's Hospital, Heidelberg, Victoria, Australiaen_US
dc.identifier.affiliationSt. Vincent's Institute of Medical Research, Fitzroy, Victoria, Australiaen_US
dc.identifier.affiliationKidney Laboratory, Institute for Breathing and Sleep, Austin Health, Heidelberg, Victoria, Australiaen_US
dc.identifier.affiliationGeneral Medicineen_US
dc.identifier.affiliationNephrologyen_US
dc.identifier.doi10.1111/iep.12313en_US
dc.type.contentTexten_US
dc.identifier.orcid0000-0003-3983-0581en_US
dc.identifier.orcid0000-0001-5838-7779en_US
dc.identifier.orcid0000-0001-7637-3661en_US
dc.identifier.pubmedid31025787-
dc.type.austinJournal Article-
local.name.researcherChoy, Suet-Wan
item.grantfulltextnone-
item.cerifentitytypePublications-
item.openairetypeJournal Article-
item.fulltextNo Fulltext-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.languageiso639-1en-
crisitem.author.deptNephrology-
crisitem.author.deptInstitute for Breathing and Sleep-
crisitem.author.deptNephrology-
crisitem.author.deptInstitute for Breathing and Sleep-
crisitem.author.deptMedicine (University of Melbourne)-
crisitem.author.deptMedicine (University of Melbourne)-
crisitem.author.deptInstitute for Breathing and Sleep-
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