Please use this identifier to cite or link to this item: https://doi.org/10.1126/science.1188280
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dc.titleSfrp5 is an anti-inflammatory adipokine that modulates metabolic dysfunction in obesity
dc.contributor.authorOuchi, N.
dc.contributor.authorHiguchi, A.
dc.contributor.authorOhashi, K.
dc.contributor.authorOshima, Y.
dc.contributor.authorGokce, N.
dc.contributor.authorShibata, R.
dc.contributor.authorAkasaki, Y.
dc.contributor.authorShimono, A.
dc.contributor.authorWalsh, K.
dc.date.accessioned2014-12-12T07:34:15Z
dc.date.available2014-12-12T07:34:15Z
dc.date.issued2010-07-23
dc.identifier.citationOuchi, N., Higuchi, A., Ohashi, K., Oshima, Y., Gokce, N., Shibata, R., Akasaki, Y., Shimono, A., Walsh, K. (2010-07-23). Sfrp5 is an anti-inflammatory adipokine that modulates metabolic dysfunction in obesity. Science 329 (5990) : 454-457. ScholarBank@NUS Repository. https://doi.org/10.1126/science.1188280
dc.identifier.issn00368075
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/115929
dc.description.abstractAdipose tissue secretes proteins referred to as adipokines, many of which promote inflammation and disrupt glucose homeostasis. Here we show that secreted frizzled-related protein 5 (Sfrp5), a protein previously linked to the Wnt signaling pathway, is an anti-inflammatory adipokine whose expression is perturbed inmodels of obesity and type 2 diabetes. Sfrp5-deficient mice fed a high-calorie diet developed severe glucose intolerance and hepatic steatosis, and their adipose tissue showed an accumulation of activated macrophages that was associated with activation of the c-Jun N-terminal kinase signaling pathway. Adenovirus-mediated delivery of Sfrp5 to mouse models of obesity ameliorated glucose intolerance and hepatic steatosis. Thus, in the setting of obesity, Sfrp5 secretion by adipocytes exerts salutary effects on metabolic dysfunction by controlling inflammatory cells within adipose tissue.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1126/science.1188280
dc.sourceScopus
dc.typeArticle
dc.contributor.departmentCANCER SCIENCE INSTITUTE OF SINGAPORE
dc.description.doi10.1126/science.1188280
dc.description.sourcetitleScience
dc.description.volume329
dc.description.issue5990
dc.description.page454-457
dc.description.codenSCIEA
dc.identifier.isiut000280196500041
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