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Loss of Krüppel-like factor 3 (KLF3/BKLF) leads to upregulation of the insulin-sensitizing factor adipolin (FAM132A/CTRP12/C1qdc2).
Loss of Krüppel-like factor 3 (KLF3/BKLF) leads to upregulation of the insulin-sensitizing factor adipolin (FAM132A/CTRP12/C1qdc2).
dc.contributor.author | Bell Anderson, Kim | en_US |
dc.contributor.author | Funnell, Alister | en_US |
dc.contributor.author | Williams, Helen | en_US |
dc.contributor.author | Mat Jusoh, H | en_US |
dc.contributor.author | Scully, T | en_US |
dc.contributor.author | Lim, Wooi | en_US |
dc.contributor.author | Burdach, John | en_US |
dc.contributor.author | Mak, Ka Sin | en_US |
dc.contributor.author | Knights, Alexander | en_US |
dc.contributor.author | Hoy, A | en_US |
dc.contributor.author | Nicholas, Hannah | en_US |
dc.contributor.author | Sainsbury, A | en_US |
dc.contributor.author | Turner, N | en_US |
dc.contributor.author | Pearson, Richard | en_US |
dc.contributor.author | Crossley, Merlin | en_US |
dc.date.accessioned | 2021-11-25T12:27:41Z | |
dc.date.available | 2021-11-25T12:27:41Z | |
dc.date.issued | 2013 | en_US |
dc.description.abstract | Krüppel-like factor 3 (KLF3) is a transcriptional regulator that we have shown to be involved in the regulation of adipogenesis in vitro. Here, we report that KLF3-null mice are lean and protected from diet-induced obesity and glucose intolerance. On a chow diet, plasma levels of leptin are decreased, and adiponectin is increased. Despite significant reductions in body weight and adiposity, wild-type and knockout animals show equivalent energy intake, expenditure, and excretion. To investigate the molecular events underlying these observations, we used microarray analysis to compare gene expression in Klf3(+/+) and Klf3(-/-) tissues. We found that mRNA expression of Fam132a, which encodes a newly identified insulin-sensitizing adipokine, adipolin, is significantly upregulated in the absence of KLF3. We confirmed that KLF3 binds the Fam132a promoter in vitro and in vivo and that this leads to repression of promoter activity. Further, plasma adipolin levels were significantly increased in Klf3(-/-) mice compared with wild-type littermates. Boosting levels of adipolin via targeting of KLF3 offers a novel potential therapeutic strategy for the treatment of insulin resistance. | en_US |
dc.identifier.issn | 0012-1797 | en_US |
dc.identifier.uri | http://hdl.handle.net/1959.4/53160 | |
dc.language | English | |
dc.language.iso | EN | en_US |
dc.rights | CC BY-NC-ND 3.0 | en_US |
dc.rights.uri | https://creativecommons.org/licenses/by-nc-nd/3.0/au/ | en_US |
dc.source | Legacy MARC | en_US |
dc.subject.other | Transcriptional regulation | en_US |
dc.subject.other | KLF3 | en_US |
dc.subject.other | Adipolin | en_US |
dc.title | Loss of Krüppel-like factor 3 (KLF3/BKLF) leads to upregulation of the insulin-sensitizing factor adipolin (FAM132A/CTRP12/C1qdc2). | en_US |
dc.type | Journal Article | en |
dcterms.accessRights | open access | |
dspace.entity.type | Publication | en_US |
unsw.accessRights.uri | https://purl.org/coar/access_right/c_abf2 | |
unsw.description.publisherStatement | This is an author-created, uncopyedited electronic version of an article accepted for publication in Diabetes. The American Diabetes Association (ADA), publisher of Diabetes, is not responsible for any errors or omissions in this version of the manuscript or any version derived from it by third parties. The definitive publisher-authenticated version will be available in a future issue of Diabetes in print and online at http://diabetes.diabetesjournals.org. | en_US |
unsw.identifier.doiPublisher | http://dx.doi.org/10.2337/db12-1745 | en_US |
unsw.relation.FunderRefNo | 632877 | en_US |
unsw.relation.FunderRefNoURL | http://purl.org/au-research/grants/nhmrc/632877 | en_US |
unsw.relation.faculty | Science | |
unsw.relation.fundingScheme | NHMRC Project | en_US |
unsw.relation.ispartofissue | 8 | en_US |
unsw.relation.ispartofjournal | Diabetes | en_US |
unsw.relation.ispartofpagefrompageto | 2728-2737 | en_US |
unsw.relation.ispartofvolume | 62 | en_US |
unsw.relation.originalPublicationAffiliation | Bell Anderson, Kim | en_US |
unsw.relation.originalPublicationAffiliation | Funnell, Alister, Biotechnology & Biomolecular Sciences, Faculty of Science, UNSW | en_US |
unsw.relation.originalPublicationAffiliation | Williams, Helen | en_US |
unsw.relation.originalPublicationAffiliation | Mat Jusoh, H | en_US |
unsw.relation.originalPublicationAffiliation | Scully, T | en_US |
unsw.relation.originalPublicationAffiliation | Lim, Wooi, Biotechnology & Biomolecular Sciences, Faculty of Science, UNSW | en_US |
unsw.relation.originalPublicationAffiliation | Burdach, John, Biotechnology & Biomolecular Sciences, Faculty of Science, UNSW | en_US |
unsw.relation.originalPublicationAffiliation | Mak, Ka Sin, Biotechnology & Biomolecular Sciences, Faculty of Science, UNSW | en_US |
unsw.relation.originalPublicationAffiliation | Knights, Alexander, Biotechnology & Biomolecular Sciences, Faculty of Science, UNSW | en_US |
unsw.relation.originalPublicationAffiliation | Hoy, A | en_US |
unsw.relation.originalPublicationAffiliation | Nicholas, Hannah | en_US |
unsw.relation.originalPublicationAffiliation | Sainsbury, A | en_US |
unsw.relation.originalPublicationAffiliation | Turner, N | en_US |
unsw.relation.originalPublicationAffiliation | Pearson, Richard, Biotechnology & Biomolecular Sciences, Faculty of Science, UNSW | en_US |
unsw.relation.originalPublicationAffiliation | Crossley, Merlin, Biotechnology & Biomolecular Sciences, Faculty of Science, UNSW | en_US |
unsw.relation.school | School of Biotechnology & Biomolecular Sciences | * |
unsw.subject.fieldofresearchcode | 060104 Cell Metabolism | en_US |
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