1215-Lipoxygenase Is Required for the Early Onset of High Fat Diet-Induced Adipose Tissue Inflammation and Insulin Resistance in Mice 英文参考文献.docVIP

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1215-Lipoxygenase Is Required for the Early Onset of High Fat Diet-Induced Adipose Tissue Inflammation and Insulin Resistance in Mice 英文参考文献.doc

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1215-Lipoxygenase Is Required for the Early Onset of High Fat Diet-Induced Adipose Tissue Inflammation and Insulin Resistance in Mice 英文参考文献

12/15-LipoxygenaseIsRequiredfortheEarlyOnsetof HighFatDiet-InducedAdiposeTissueInflammationand InsulinResistanceinMice DorothyD.Sears1*,PhilipD.Miles1,JustinChapman2,JachelleM.Ofrecio1,FelicidadAlmazan1 ,Divya Thapar1,YuryI.Miller1 1DivisionofEndocrinologyandMetabolism,DepartmentofMedicine,UniversityofCaliforniaSanDiego,LaJolla,California,UnitedStatesofAmerica,2PfizerInc.,LaJolla, California,UnitedStatesofAmerica Abstract Background: Recent understandingthatinsulinresistanceis aninflammatoryconditionnecessitatessearching forgenes that regulate inflammation in insulin sensitive tissues. 12/15-lipoxygenase (12/15LO) regulates the expression of proinflammatory cytokines and chemokines and is implicated in the early development of diet-induced atherosclerosis. Thus,wetestedthehypothesisthat12/15LOisinvolvedintheonsetofhighfatdiet(HFD)-inducedinsulinresistance. Methodology/PrincipalFindings:Cellsover-expressing12/15LOsecretedtwopotentchemokines,MCP-1andosteopontin, implicated in the development of insulin resistance. We assessed adipose tissue inflammation and whole body insulin resistanceinwildtype(WT)and12/15LOknockout(KO)miceafter2–4weeksonHFD.InadiposetissuefromWTmice,HFD resultedinrecruitmentofCD11b+,F4/80+macrophagesandelevatedproteinlevelsoftheinflammatorymarkersIL-1b ,IL-6, IL-10, IL-12, IFNc, Cxcl1 and TNFa. Remarkably, adipose tissue from HFD-fed 12/15LO KO mice was not infiltrated by macrophagesanddidnotdisplayanyincreaseintheinflammatorymarkerscomparedtoadiposetissuefromnormalchow- fedmice.WTmicedevelopedseverewholebody(hepaticandskeletalmuscle)insulinresistanceafterHFD,asmeasuredby hyperinsulinemiceuglycemicclamp.Incontrast,12/15LOKOmiceexhibitednoHFD-inducedchangeininsulin-stimulated glucose disposal rate or hepatic glucose output during clamp studies. Insulin-stimulated Akt phosphorylation in muscle tissuefromHFD-fedmicewassignificantlygreaterin12/15LOKOmicethaninWTmice. Conclusions:Theseresultsdemonstratethat12/15LOmediatesearlystagesofadiposetissue