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dc.contributor.authorDagdeviren, Sezin
dc.contributor.authorJung, Dae Young
dc.contributor.authorFriedline, Randall H.
dc.contributor.authorNoh, Hye Lim
dc.contributor.authorKim, Jong Hun
dc.contributor.authorPatel, Payal R.
dc.contributor.authorTsitsilianos, Nicholas
dc.contributor.authorInashima, Kunikazu
dc.contributor.authorTran, Duy A.
dc.contributor.authorHu, Xiaodi
dc.contributor.authorLoubato, Marilia M.
dc.contributor.authorCraige, Siobhan M.
dc.contributor.authorKwon, Jung Yeon
dc.contributor.authorLee, Ki Won.
dc.contributor.authorKim, Jason K.
dc.date2022-08-11T08:08:19.000
dc.date.accessioned2022-08-23T15:51:03Z
dc.date.available2022-08-23T15:51:03Z
dc.date.issued2016-11-03
dc.date.submitted2016-12-06
dc.identifier.citationFASEB J. 2016 Nov 3. pii: fj.201600832R. <a href="http://dx.doi.org/10.1096/fj.201600832R">Link to article on publisher's site</a>
dc.identifier.issn0892-6638 (Linking)
dc.identifier.doi10.1096/fj.201600832R
dc.identifier.pmid27811060
dc.identifier.urihttp://hdl.handle.net/20.500.14038/28805
dc.description.abstractAltered energy balance and insulin resistance are important characteristics of aging. Skeletal muscle is a major site of glucose disposal, and the role of aging-associated inflammation in skeletal muscle insulin resistance remains unclear. To investigate, we examined glucose metabolism in 18-mo-old transgenic mice with muscle-specific overexpression of IL-10 (MIL10) and in wild-type mice during hyperinsulinemic-euglycemic clamping. Despite similar fat mass and energy balance, MIL10 mice were protected from aging-associated insulin resistance with significant increases in glucose infusion rates, whole-body glucose turnover, and skeletal muscle glucose uptake ( approximately 60%; P < 0.05), as compared to age-matched WT mice. This protective effect was associated with decreased muscle inflammation, but no changes in adipose tissue inflammation in aging MIL10 mice. These results demonstrate the importance of skeletal muscle inflammation in aging-mediated insulin resistance, and our findings further implicate a potential therapeutic role of anti-inflammatory cytokine in the treatment of aging-mediated insulin resistance.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=27811060&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1096/fj.201600832R
dc.subjectcytokines
dc.subjectinterleukins
dc.subjectaging
dc.subjecttype 2 diabetes
dc.subjectglucose metabolism
dc.subjectCellular and Molecular Physiology
dc.subjectEndocrinology
dc.subjectEndocrinology, Diabetes, and Metabolism
dc.titleIL-10 prevents aging-associated inflammation and insulin resistance in skeletal muscle
dc.typeJournal Article
dc.source.journaltitleFASEB journal : official publication of the Federation of American Societies for Experimental Biology
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/faculty_pubs/1043
dc.identifier.contextkey9445252
html.description.abstract<p>Altered energy balance and insulin resistance are important characteristics of aging. Skeletal muscle is a major site of glucose disposal, and the role of aging-associated inflammation in skeletal muscle insulin resistance remains unclear. To investigate, we examined glucose metabolism in 18-mo-old transgenic mice with muscle-specific overexpression of IL-10 (MIL10) and in wild-type mice during hyperinsulinemic-euglycemic clamping. Despite similar fat mass and energy balance, MIL10 mice were protected from aging-associated insulin resistance with significant increases in glucose infusion rates, whole-body glucose turnover, and skeletal muscle glucose uptake ( approximately 60%; P < 0.05), as compared to age-matched WT mice. This protective effect was associated with decreased muscle inflammation, but no changes in adipose tissue inflammation in aging MIL10 mice. These results demonstrate the importance of skeletal muscle inflammation in aging-mediated insulin resistance, and our findings further implicate a potential therapeutic role of anti-inflammatory cytokine in the treatment of aging-mediated insulin resistance.</p>
dc.identifier.submissionpathfaculty_pubs/1043
dc.contributor.departmentDepartment of Medicine, Division of Cardiovascular Medicine
dc.contributor.departmentProgram in Molecular Medicine


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