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dc.contributor.authorPan, Dongning
dc.contributor.authorMao, Chunxiao
dc.contributor.authorQuattrochi, Brian
dc.contributor.authorFriedline, Randall H.
dc.contributor.authorZhu, Lihua Julie
dc.contributor.authorJung, Dae Young
dc.contributor.authorKim, Jason K.
dc.contributor.authorLewis, Brian C.
dc.contributor.authorWang, Yong-Xu
dc.date2022-08-11T08:10:15.000
dc.date.accessioned2022-08-23T17:01:38Z
dc.date.available2022-08-23T17:01:38Z
dc.date.issued2014-08-22
dc.date.submitted2014-11-04
dc.identifier.citationNat Commun. 2014 Aug 22;5:4725. doi: 10.1038/ncomms5725. <a href="http://dx.doi.org/10.1038/ncomms5725">Link to article on publisher's site</a>
dc.identifier.issn2041-1723 (Linking)
dc.identifier.doi10.1038/ncomms5725
dc.identifier.pmid25145289
dc.identifier.urihttp://hdl.handle.net/20.500.14038/44049
dc.description.abstractBoth classical brown adipocytes and brown-like beige adipocytes are considered as promising therapeutic targets for obesity; however, their development, relative importance and functional coordination are not well understood. Here we show that a modest expression of miR-378/378* in adipose tissue specifically increases classical brown fat (BAT) mass, but not white fat (WAT) mass. Remarkably, BAT expansion, rather than miR-378 per se, suppresses formation of beige adipocytes in subcutaneous WAT. Despite this negative feedback, the expanded BAT depot is sufficient to prevent both genetic and high-fat diet-induced obesity. At the molecular level, we find that miR-378 targets phosphodiesterase Pde1b in BAT but not in WAT. Indeed, miR-378 and Pde1b inversely regulate brown adipogenesis in vitro in the absence of phosphodiesterase inhibitor isobutylmethylxanthine. Our work identifies miR-378 as a key regulatory component underlying classical BAT-specific expansion and obesity resistance, and adds novel insights into the physiological crosstalk between BAT and WAT.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=25145289&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1038/ncomms5725
dc.subjectCellular and Molecular Physiology
dc.subjectMolecular Biology
dc.subjectMolecular Genetics
dc.titleMicroRNA-378 controls classical brown fat expansion to counteract obesity
dc.typeJournal Article
dc.source.journaltitleNature communications
dc.source.volume5
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/pgfe_pp/264
dc.legacy.embargo2014-11-06T00:00:00-08:00
dc.identifier.contextkey6324041
html.description.abstract<p>Both classical brown adipocytes and brown-like beige adipocytes are considered as promising therapeutic targets for obesity; however, their development, relative importance and functional coordination are not well understood. Here we show that a modest expression of miR-378/378* in adipose tissue specifically increases classical brown fat (BAT) mass, but not white fat (WAT) mass. Remarkably, BAT expansion, rather than miR-378 per se, suppresses formation of beige adipocytes in subcutaneous WAT. Despite this negative feedback, the expanded BAT depot is sufficient to prevent both genetic and high-fat diet-induced obesity. At the molecular level, we find that miR-378 targets phosphodiesterase Pde1b in BAT but not in WAT. Indeed, miR-378 and Pde1b inversely regulate brown adipogenesis in vitro in the absence of phosphodiesterase inhibitor isobutylmethylxanthine. Our work identifies miR-378 as a key regulatory component underlying classical BAT-specific expansion and obesity resistance, and adds novel insights into the physiological crosstalk between BAT and WAT.</p>
dc.identifier.submissionpathpgfe_pp/264
dc.contributor.departmentProgram in Molecular Medicine
dc.contributor.departmentProgram in Gene Function and Expression
dc.source.pages4725


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