Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/10582
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dc.contributor.authorMacLean, Helen Een
dc.contributor.authorChiu, W S Mariaen
dc.contributor.authorNotini, Amanda Jen
dc.contributor.authorAxell, Anna-Mareeen
dc.contributor.authorDavey, Rachel Aen
dc.contributor.authorMcManus, Julie Fen
dc.contributor.authorMa, Cathyen
dc.contributor.authorPlant, David Ren
dc.contributor.authorLynch, Gordon Sen
dc.contributor.authorZajac, Jeffrey Den
dc.date.accessioned2015-05-16T00:05:15Z
dc.date.available2015-05-16T00:05:15Z
dc.date.issued2008-04-07en
dc.identifier.citationFaseb Journal : Official Publication of the Federation of American Societies For Experimental Biology 2008; 22(8): 2676-89en
dc.identifier.govdoc18390925en
dc.identifier.otherPUBMEDen
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/10582en
dc.description.abstractTo identify mechanisms of anabolic androgen action in muscle, we generated male and female genomic androgen receptor (AR) knockout (ARKO) mice, and characterized muscle mass, contractile function, and gene expression. Muscle mass is decreased in ARKO males, but normal in ARKO females. The levator ani muscle, which fails to develop in normal females, is also absent in ARKO males. Force production is decreased from fast-twitch ARKO male muscle, and slow-twitch muscle has increased fatigue resistance. Microarray analysis shows up-regulation of genes encoding slow-twitch muscle contractile proteins. Real-time PCR confirms that expression of genes encoding polyamine biosynthetic enzymes, ornithine decarboxylase (Odc1), and S-adenosylmethionine decarboxylase (Amd1), is reduced in ARKO muscle, suggesting androgens act through regulation of polyamine biosynthesis. Altered expression of regulators of myoblast progression from proliferation to terminal differentiation suggests androgens also promote muscle growth by maintaining myoblasts in the proliferate state and delaying differentiation (increased Cdkn1c and Igf2, decreased Itg1bp3). A similar pattern of gene expression is observed in orchidectomized male mice, during androgen withdrawal-dependent muscle atrophy. In conclusion, androgens are not required for peak muscle mass in females. In males, androgens act through the AR to regulate multiple gene pathways that control muscle mass, strength, and fatigue resistance.en
dc.language.isoenen
dc.subject.otherAndrogens.physiologyen
dc.subject.otherAnimalsen
dc.subject.otherCell Differentiationen
dc.subject.otherCell Proliferationen
dc.subject.otherFemaleen
dc.subject.otherGene Expressionen
dc.subject.otherGene Regulatory Networksen
dc.subject.otherMaleen
dc.subject.otherMiceen
dc.subject.otherMice, Inbred C57BLen
dc.subject.otherMice, Knockouten
dc.subject.otherMuscle Contraction.physiologyen
dc.subject.otherMuscle Fibers, Fast-Twitch.physiologyen
dc.subject.otherMuscle Fibers, Slow-Twitch.physiologyen
dc.subject.otherMuscle, Skeletal.growth & development.pathology.physiopathologyen
dc.subject.otherMyoblasts, Skeletal.pathology.physiologyen
dc.subject.otherOrchiectomyen
dc.subject.otherOrgan Sizeen
dc.subject.otherReceptors, Androgen.deficiency.genetics.physiologyen
dc.subject.otherSex Characteristicsen
dc.subject.otherTestis.physiologyen
dc.titleImpaired skeletal muscle development and function in male, but not female, genomic androgen receptor knockout mice.en
dc.typeJournal Articleen
dc.identifier.journaltitleFASEB journal : official publication of the Federation of American Societies for Experimental Biologyen
dc.identifier.affiliationDepartment of Medicine, Austin Health, The University of Melbourne, Heidelberg, Victoria, Australiaen
dc.identifier.doi10.1096/fj.08-105726en
dc.description.pages2676-89en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/18390925en
dc.type.austinJournal Articleen
local.name.researcherZajac, Jeffrey D
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
item.fulltextNo Fulltext-
item.grantfulltextnone-
item.languageiso639-1en-
item.openairetypeJournal Article-
crisitem.author.deptEndocrinology-
crisitem.author.deptMedicine (University of Melbourne)-
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