Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/11528
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dc.contributor.authorFam, Barbara Cen
dc.contributor.authorRose, Laura Jen
dc.contributor.authorSgambellone, Rebeccaen
dc.contributor.authorRuan, Zhengen
dc.contributor.authorProietto, Josephen
dc.contributor.authorAndrikopoulos, Sofianosen
dc.date.accessioned2015-05-16T01:08:31Z
dc.date.available2015-05-16T01:08:31Z
dc.date.issued2012-06-26en
dc.identifier.citationThe Journal of Endocrinology 2012; 214(3): 313-27en
dc.identifier.govdoc22736482en
dc.identifier.otherPUBMEDen
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/11528en
dc.description.abstractSkeletal muscle insulin resistance is a major characteristic underpinning type 2 diabetes. Impairments in the insulin responsiveness of the glucose transporter, Glut4 (Slc2a4), have been suggested to be a contributing factor to this disturbance. We have produced muscle-specific Glut4 knockout (KO) mice using Cre/LoxP technology on a C57BL6/J background and shown undetectable levels of GLUT4 in both skeletal muscle and heart. Our aim was to determine whether complete deletion of muscle GLUT4 does in fact lead to perturbations in glucose homoeostasis. Glucose tolerance, glucose turnover and 2-deoxyglucose uptake into muscle and fat under basal and insulin-stimulated conditions were assessed in 12-week-old KO and control mice using the oral glucose tolerance test (OGTT) and hyperinsulinaemic/euglycaemic clamp respectively. KO mice weighed ~17% less and had significantly heavier hearts compared with control mice. Basally, plasma glucose and plasma insulin were significantly lower in the KO compared with control mice, which conferred normal glucose tolerance. Despite the lack of GLUT4 in the KO mouse muscle, glucose uptake was not impaired in skeletal muscle but was reduced in heart under insulin-stimulated conditions. Neither GLUT1 nor GLUT12 protein levels were altered in the skeletal muscle or heart tissue of our KO mice. High-fat feeding did not alter glucose tolerance in the KO mice but led to elevated plasma insulin levels during the glucose tolerance test. Our study demonstrates that deletion of muscle GLUT4 does not adversely affect glucose disposal and glucose tolerance and that compensation from other transporters may contribute to this unaltered homoeostasis of glucose.en
dc.language.isoenen
dc.subject.otherAnimalsen
dc.subject.otherBlood Glucose.metabolismen
dc.subject.otherDiabetes Mellitus, Type 2.genetics.metabolismen
dc.subject.otherDietary Fats.pharmacologyen
dc.subject.otherFemaleen
dc.subject.otherGenes, Homeobox.physiologyen
dc.subject.otherGlucose Clamp Techniqueen
dc.subject.otherGlucose Intolerance.genetics.metabolismen
dc.subject.otherGlucose Tolerance Testen
dc.subject.otherGlucose Transport Proteins, Facilitative.genetics.metabolismen
dc.subject.otherGlucose Transporter Type 1.genetics.metabolismen
dc.subject.otherGlucose Transporter Type 4.genetics.metabolismen
dc.subject.otherIntegrases.geneticsen
dc.subject.otherMaleen
dc.subject.otherMiceen
dc.subject.otherMice, Inbred C57BLen
dc.subject.otherMice, Knockouten
dc.subject.otherMuscle, Skeletal.metabolismen
dc.subject.otherPregnancyen
dc.subject.otherRNA, Messenger.metabolismen
dc.titleNormal muscle glucose uptake in mice deficient in muscle GLUT4.en
dc.typeJournal Articleen
dc.identifier.journaltitleThe Journal of Endocrinologyen
dc.identifier.affiliationDepartment of Medicine (Austin Health), Austin Hospital, University of Melbourne, Heidelberg, Victoria 3084, Australiaen
dc.identifier.doi10.1530/JOE-12-0032en
dc.description.pages313-27en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/22736482en
dc.type.austinJournal Articleen
local.name.researcherProietto, Joseph
item.fulltextNo Fulltext-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.languageiso639-1en-
item.openairetypeJournal Article-
item.grantfulltextnone-
item.cerifentitytypePublications-
crisitem.author.deptMedicine (University of Melbourne)-
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