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dc.contributor.authorSanchez-Gurmaches, Joan
dc.contributor.authorGuertin, David A.
dc.date2022-08-11T08:10:18.000
dc.date.accessioned2022-08-23T17:03:36Z
dc.date.available2022-08-23T17:03:36Z
dc.date.issued2014-06-19
dc.date.submitted2016-04-13
dc.identifier.citationNat Commun. 2014 Jun 19;5:4099. doi: 10.1038/ncomms5099. <a href="http://dx.doi.org/10.1038/ncomms5099">Link to article on publisher's site</a>
dc.identifier.issn2041-1723 (Linking)
dc.identifier.doi10.1038/ncomms5099
dc.identifier.pmid24942009
dc.identifier.urihttp://hdl.handle.net/20.500.14038/44460
dc.description.abstractAdipose tissue development is poorly understood. Here we use a lineage-tracing strategy optimal for adipocytes to provide evidence that Myf5 precursors are not the exclusive source of brown adipocytes and contribute more to the mature white and brite adipocyte populations than previously thought. Moreover, Myf5-lineage distribution in adipose tissue changes in response to modifiable and non-modifiable factors. We also find that the Pax3 lineage largely overlaps with the Myf5 lineage in brown fat and subcutaneous white fat, but exhibits gender-linked divergence in visceral white fat while the MyoD1 lineage does not give rise to any adipocytes. Finally, by deleting insulin receptor beta in the Myf5 lineage, we provide in vivo evidence that the insulin receptor is essential for adipogenesis and that adipocyte lineages have plasticity. These data establish a conceptual framework for adipose tissue development and could explain body fat patterning variations in healthy and lipodystrophic or obese humans.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=24942009&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC4066194/
dc.subjectAdipocytes
dc.subjectAdipogenesis
dc.subjectAdipose Tissue, Brown
dc.subjectAdipose Tissue, White
dc.subjectAnimals
dc.subject*Cell Lineage
dc.subjectFemale
dc.subjectMale
dc.subjectMice
dc.subjectMyoD Protein
dc.subjectMyogenic Regulatory Factor 5
dc.subjectReceptor, Insulin
dc.subjectCell Biology
dc.subjectDevelopmental Biology
dc.titleAdipocytes arise from multiple lineages that are heterogeneously and dynamically distributed
dc.typeJournal Article
dc.source.journaltitleNature communications
dc.source.volume5
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=1053&amp;context=pmm_pp&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/pmm_pp/54
dc.identifier.contextkey8471538
refterms.dateFOA2022-08-23T17:03:36Z
html.description.abstract<p>Adipose tissue development is poorly understood. Here we use a lineage-tracing strategy optimal for adipocytes to provide evidence that Myf5 precursors are not the exclusive source of brown adipocytes and contribute more to the mature white and brite adipocyte populations than previously thought. Moreover, Myf5-lineage distribution in adipose tissue changes in response to modifiable and non-modifiable factors. We also find that the Pax3 lineage largely overlaps with the Myf5 lineage in brown fat and subcutaneous white fat, but exhibits gender-linked divergence in visceral white fat while the MyoD1 lineage does not give rise to any adipocytes. Finally, by deleting insulin receptor beta in the Myf5 lineage, we provide in vivo evidence that the insulin receptor is essential for adipogenesis and that adipocyte lineages have plasticity. These data establish a conceptual framework for adipose tissue development and could explain body fat patterning variations in healthy and lipodystrophic or obese humans.</p>
dc.identifier.submissionpathpmm_pp/54
dc.contributor.departmentProgram in Molecular Medicine
dc.source.pages4099


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