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dc.contributor.authorAouadi, Myriam
dc.contributor.authorTencerova, Michaela
dc.contributor.authorVangala, Pranitha
dc.contributor.authorYawe, Joseph
dc.contributor.authorNicoloro, Sarah M.
dc.contributor.authorAmano, Shinya U.
dc.contributor.authorCohen, Jessica L.
dc.contributor.authorCzech, Michael P.
dc.date2022-08-11T08:08:28.000
dc.date.accessioned2022-08-23T15:56:05Z
dc.date.available2022-08-23T15:56:05Z
dc.date.issued2013-05-14
dc.date.submitted2013-06-05
dc.identifier.citation<p>Proc Natl Acad Sci U S A. 2013 May 14;110(20):8278-83. doi: 10.1073/pnas.1300492110. <a href="http://dx.doi.org/10.1073/pnas.1300492110">Link to article on publisher's site</a></p>
dc.identifier.issn0027-8424 (Linking)
dc.identifier.doi10.1073/pnas.1300492110
dc.identifier.pmid23630254
dc.identifier.urihttp://hdl.handle.net/20.500.14038/29894
dc.description.abstractAdipose tissue (AT) inflammation and infiltration by macrophages is associated with insulin resistance and type 2 diabetes in obese humans, offering a potential target for therapeutics. However, whether AT macrophages (ATMs) directly contribute to systemic glucose intolerance has not been determined. The reason is the lack of methods to ablate inflammatory genes expressed in macrophages specifically localized within AT depots, leaving macrophages in other tissues unaffected. Here we report that i.p. administration of siRNA encapsulated by glucan shells in obese mice selectively silences genes in epididymal ATMs, whereas macrophages within lung, spleen, kidney, heart, skeletal muscle, subcutaneous (SubQ) adipose, and liver are not targeted. Such administration of GeRPs to silence the inflammatory cytokines TNF-alpha or osteopontin in epididymal ATMs of obese mice caused significant improvement in glucose tolerance. These data are consistent with the hypothesis that cytokines produced by ATMs can exacerbate whole-body glucose intolerance.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=23630254&dopt=Abstract">Link to Article in PubMed</a></p>
dc.relation.urlhttp://dx.doi.org/10.1073/pnas.1300492110
dc.subjectObesity
dc.subjectGene Silencing
dc.subjectRNA Interference
dc.subjectAdipose Tissue
dc.subjectMacrophages
dc.subjectGlucose Intolerance
dc.subjectGenetics and Genomics
dc.subjectNutritional and Metabolic Diseases
dc.subjectPhysiology
dc.titleGene silencing in adipose tissue macrophages regulates whole-body metabolism in obese mice
dc.typeJournal Article
dc.source.journaltitleProceedings of the National Academy of Sciences of the United States of America
dc.source.volume110
dc.source.issue20
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/faculty_pubs/21
dc.identifier.contextkey4199951
html.description.abstract<p>Adipose tissue (AT) inflammation and infiltration by macrophages is associated with insulin resistance and type 2 diabetes in obese humans, offering a potential target for therapeutics. However, whether AT macrophages (ATMs) directly contribute to systemic glucose intolerance has not been determined. The reason is the lack of methods to ablate inflammatory genes expressed in macrophages specifically localized within AT depots, leaving macrophages in other tissues unaffected. Here we report that i.p. administration of siRNA encapsulated by glucan shells in obese mice selectively silences genes in epididymal ATMs, whereas macrophages within lung, spleen, kidney, heart, skeletal muscle, subcutaneous (SubQ) adipose, and liver are not targeted. Such administration of GeRPs to silence the inflammatory cytokines TNF-alpha or osteopontin in epididymal ATMs of obese mice caused significant improvement in glucose tolerance. These data are consistent with the hypothesis that cytokines produced by ATMs can exacerbate whole-body glucose intolerance.</p>
dc.identifier.submissionpathfaculty_pubs/21
dc.contributor.departmentProgram in Molecular Medicine
dc.source.pages8278-83


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