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dc.contributor.authorNam, Minwoo
dc.contributor.authorCooper, Marcus P.
dc.date2022-08-11T08:09:44.000
dc.date.accessioned2022-08-23T16:41:37Z
dc.date.available2022-08-23T16:41:37Z
dc.date.issued2015-06-30
dc.date.submitted2016-04-25
dc.identifier.citationFront Endocrinol (Lausanne). 2015 Jun 30;6:104. doi: 10.3389/fendo.2015.00104. eCollection 2015. <a href="http://dx.doi.org/10.3389/fendo.2015.00104">Link to article on publisher's site</a>
dc.identifier.issn1664-2392 (Linking)
dc.identifier.doi10.3389/fendo.2015.00104
dc.identifier.pmid26175716
dc.identifier.urihttp://hdl.handle.net/20.500.14038/39921
dc.description.abstractIn murine and human brown adipose tissue (BAT), mitochondria are powerful generators of heat that safely metabolize fat, a feature that has great promise in the fight against obesity and diabetes. Recent studies suggest that the actions of mitochondria extend beyond their conventional role as generators of heat. There is mounting evidence that impaired mitochondrial respiratory capacity is accompanied by attenuated expression of Ucp1 and other BAT-selective genes, implying that mitochondria exert transcriptional control over the brown fat gene program. In this review, we discuss the current understanding of brown fat mitochondria, their potential role in transcriptional control of the brown fat gene program, and potential strategies to treat obesity in humans by leveraging thermogenesis in brown adipocytes.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=26175716&dopt=Abstract">Link to Article in PubMed</a>
dc.rightsCopyright © 2015 Nam and Cooper. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectbrown fat
dc.subjectbrown fat gene program
dc.subjectmitochondria
dc.subjectrespiratory capacity
dc.subjectthermogenesis
dc.subjectEndocrinology
dc.subjectEndocrinology, Diabetes, and Metabolism
dc.titleRole of Energy Metabolism in the Brown Fat Gene Program
dc.typeJournal Article
dc.source.journaltitleFrontiers in endocrinology
dc.source.volume6
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=3732&amp;context=oapubs&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/2728
dc.identifier.contextkey8515410
refterms.dateFOA2022-08-23T16:41:37Z
html.description.abstract<p>In murine and human brown adipose tissue (BAT), mitochondria are powerful generators of heat that safely metabolize fat, a feature that has great promise in the fight against obesity and diabetes. Recent studies suggest that the actions of mitochondria extend beyond their conventional role as generators of heat. There is mounting evidence that impaired mitochondrial respiratory capacity is accompanied by attenuated expression of Ucp1 and other BAT-selective genes, implying that mitochondria exert transcriptional control over the brown fat gene program. In this review, we discuss the current understanding of brown fat mitochondria, their potential role in transcriptional control of the brown fat gene program, and potential strategies to treat obesity in humans by leveraging thermogenesis in brown adipocytes.</p>
dc.identifier.submissionpathoapubs/2728
dc.contributor.departmentDepartment of Medicine, Division of Cardiovascular Medicine
dc.source.pages104


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Copyright © 2015 Nam and Cooper.  This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
Except where otherwise noted, this item's license is described as Copyright © 2015 Nam and Cooper. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.