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dc.contributor.authorNicholls, HT
dc.contributor.authorKowalski, G
dc.contributor.authorKennedy, DJ
dc.contributor.authorRisis, S
dc.contributor.authorZaffino, LA
dc.contributor.authorWatson, N
dc.contributor.authorKanellakis, P
dc.contributor.authorWatt, MJ
dc.contributor.authorBobik, A
dc.contributor.authorBonen, A
dc.contributor.authorFebbraio, M
dc.contributor.authorLancaster, GI
dc.contributor.authorFebbraio, MA
dc.date.accessioned2020-12-09T23:03:46Z
dc.date.available2020-12-09T23:03:46Z
dc.date.issued2011-04-01
dc.identifierpii: db10-1353
dc.identifier.citationNicholls, H. T., Kowalski, G., Kennedy, D. J., Risis, S., Zaffino, L. A., Watson, N., Kanellakis, P., Watt, M. J., Bobik, A., Bonen, A., Febbraio, M., Lancaster, G. I. & Febbraio, M. A. (2011). Hematopoietic Cell-Restricted Deletion of CD36 Reduces High-Fat Diet-Induced Macrophage Infiltration and Improves Insulin Signaling in Adipose Tissue. DIABETES, 60 (4), pp.1100-1110. https://doi.org/10.2337/db10-1353.
dc.identifier.issn0012-1797
dc.identifier.urihttp://hdl.handle.net/11343/253132
dc.description.abstractOBJECTIVE: The fatty acid translocase and scavenger receptor CD36 is important in the recognition and uptake of lipids. Accordingly, we hypothesized that it plays a role in saturated fatty acid-induced macrophage lipid accumulation and proinflammatory activation. RESEARCH DESIGN AND METHODS: In vitro, the effect of CD36 inhibition and deletion in lipid-induced macrophage inflammation was assessed using the putative CD36 inhibitor, sulfosuccinimidyl oleate (SSO), and bone marrow-derived macrophages from mice with (CD36KO) or without (wild-type) global deletion of CD36. To investigate whether deletion of macrophage CD36 would improve insulin sensitivity in vivo, wild-type mice were transplanted with bone marrow from CD36KO or wild-type mice and then fed a standard or high-fat diet (HFD) for 20 weeks. RESULTS: SSO treatment markedly reduced saturated fatty acid-induced lipid accumulation and inflammation in RAW264.7 macrophages. Mice harboring CD36-specific deletion in hematopoietic-derived cells (HSC CD36KO) fed an HFD displayed improved insulin signaling and reduced macrophage infiltration in adipose tissue compared with wild-type mice, but this did not translate into protection against HFD-induced whole-body insulin resistance. Contrary to our hypothesis and our results using SSO in RAW264.7 macrophages, neither saturated fatty acid-induced lipid accumulation nor inflammation was reduced when comparing CD36KO with wild-type bone marrow-derived macrophages. CONCLUSIONS: Although CD36 does not appear important in saturated fatty acid-induced macrophage lipid accumulation, our study uncovers a novel role for CD36 in the migration of proinflammatory phagocytes to adipose tissue in obesity, with a concomitant improvement in insulin action.
dc.languageEnglish
dc.publisherAMER DIABETES ASSOC
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/4.0
dc.titleHematopoietic Cell-Restricted Deletion of CD36 Reduces High-Fat Diet-Induced Macrophage Infiltration and Improves Insulin Signaling in Adipose Tissue
dc.typeJournal Article
dc.identifier.doi10.2337/db10-1353
melbourne.affiliation.departmentPhysiology
melbourne.source.titleDiabetes
melbourne.source.volume60
melbourne.source.issue4
melbourne.source.pages1100-1110
dc.rights.licenseCC BY-NC-ND
melbourne.elementsid1304162
melbourne.contributor.authorWatt, Matthew
dc.identifier.eissn1939-327X
melbourne.accessrightsOpen Access


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