- 姓名:徐爱民
- 性别:男
- 出生年月:1965.2
- 专业技术职务:教授
- 专业:病理生理学
- 导师层次:博士生导师
- 导师类别:学术型
- 最后学历:博士
- 工作单位:香港大学医学院HBHA中心
- 办公室电话:85228199754
- 电子邮件:amxu@hkucc.hku.hk
Diabetes.4.JournalofObesity.AsaneditorforBiochemicalJournal(ajournalwith120yearsof
history),Iamhandling~25-30manuscriptsperyearrelatedtoobesity,energymetabolismand
signaltransduction.
2.Asaninvitedreviewerforover20journals,includingDiabetes,Am.J.ofPathology,Obesity,
ATVB,Clin.Chem,Am.J.Cardiology,Obesity,Molecularandcellularendocrinology,Physiology
Genomics,Toxicity,Journalofphysiology,InternationalJournalofBiochemistryandcellbiology,
AmJPhysiol,ClinScience,Nephrology,CellResearch,Proteomicsetc.Inthelasttwoyears,I
reviewed46manuscriptsforthesejournals.
3.AsaninvitedgrantreviewerforDiabetesUK,HongKongRGCandNewZealandHealth
ResearchGrant.
2、APPL1counteractsobesity-inducedvascularinsulinresistanceandendothelialdysfunctionbymodulatingtheendothelialproductionofnitricoxideandendothelin-1inmice,Diabetes,2011,60:3044-54,IF:8.889。
3、AdiponectinIsRequiredforPPARγ-MediatedImprovementofEndothelialFunctioninDiabeticMice,CellMetabolism,2011,16:101-15,IF:18.207。
4、AdiponectinPreventsDiabeticPrematureSenescenceofEndothelialProgenitorCellsandPromotesEndothelialRepairbySuppressingthep38MAPkinase/p16INK4ASignalingPathway,Diabetes,2010,59:2949-59,IF:8.889。
5、APPL1PotentiatesInsulin-mediatedInhibitionofHepaticGlucoseProductionandAlleviatesDiabetesviaAktActivationinMice,CellMetabolism,2009,9:417-27,IF:18.207。
1.Phosphoproteintargetforinsulinandinsulinantagonists.(USpatentnumber:US6,884,575)
2.Adiponectinandusesthereof.(USpatentNumber:7,365,170)
3.Lipocalin-2asadiagnosticmarkerandtherapeutictarget.USpatentNo:7,645,616.
B:Patentinapplicationasaninventor(5)
1.FALPproteins.(InternationalApplicationNo:PCT/NZ03/00039,US20050074756,USutility
applicationfiled03/03/2003)
2..PeptideswithAnti-ObesityActivityandOtherRelatedUses,USpatentapplicationNo:
20070275872
3.MethodforDecreasingBloodGlucoseandImprovingGlucoseToleranceUsingAngiopoietin-
Protein4.USPatentApplicationNumber:20080095782.
4.Lipocalin-2asaprognosticanddiagnosticmarkerforheartandstrokerisks.USpatentapplication
20090274709
2.BestdoctoralThesis,UniversityofAuckland,2000
2、APPL2asaNegativeRegulatorofInsulinSensitivityandGlucoseUptakeinSkeletalMuscle:ANovelPathwayLeadingtoInsulinResistance?(783010M),GeneralResearchFund,2011~2013,HK$1,380,000。
本人目前可支配总经费:HK$2,817,500。
Myresearchisdedicatedtodelineatethemolecularbasisthatlinksobesitywithdiabetesand
cardiovasculardisease,withparticularfocusesonadipokinesreleasedfromfattissue.Ourteamisone
ofthewordleadinggroupsinthefieldofadiponectin,amajorfat-derivedinsulin-sensitizing
adipokinewithanti-diabetic,anti-atheroscleroticandanti-inflammatoryproperties.Ourresearchwork
contributedsubstantiallytotheunderstandingofthemolecularstructure,signalingpathwaysand
physiologicalfunctionsofadiponectin.Severalkeyfindingsreportedfromourlaboratory,including
theposttranslationalmodificationinregulatingoligomerizationandsecretionofadiponectin,the
sexualdimorphismofadiponectin,andtheprotectiveroleofadiponectinagainstobesity-relatedfatty
liverandbreastcancer,havebeenwidelyacceptedandextensivelycitedinthisfield.Inthepastsix
year,ourgroup,incollaborationwithseveraloverseasinstitutes,haspublished42papersrelatedto
adiponectinintop-rankedjournals,includingCellMetabolism,JClinInvest,PNAS,Gastroenterology,
Hepatology,Diabetes,CancerResearch,AmJPathol,andJBC(6)etc(seethepublicationlistbelow).
Wehaveprovidedtheresearchtoolsgeneratedinourlaboratory(antibodies,celllines,immunoassays,
virusesandrecombinantadiponectinetc)toover30localandoverseaslaboratoriestosupporttheir
research.Ihavebeeninvitedtocontributereviewpapersbyseveralprestigiousjournals,including
BiochemicalJ,ClinScience,andExpertReviewinEndocrinology&Metabolismetc.
Inadditiontoadiponectin,ourlaboratoryhasidentifiedseveralothernewadipokines,
includingadipocytefattyacidbindingprotein(A-FABP),FGF21,Angptl4andlipocalin-2.Wehave
comprehensivelyinvestigatedthephysiologicalfunctionsoftheseadipokinesinanimalmodelsand
theclinicalrelevanceinhumans.Thediscoveryofthesenewadipokinesbyourgroupuncoversnovel
molecularlinksbetweenobesityanditsmetabolicandcardiovascularcomplications,andprovidesnewtargetsfortherapeuticinterventionandearlydiagnosis.Thispartofworkledto15publicationsintop
journals,includingCirculation,Diabetes,DiabetesCare(2),EuropeanHeartJ,Hepatology,Clin
Chemistry(2),PNASandATVBetc.Inaddition,wearealsousingthetransgenesisapproachesto
understandtheroleandmechanismsofadiposetissueinflammationinthepathogenesisofobesity-
inducedinsulinresistanceandvasculardysfunction.Wehavegeneratedseveralunique
transgenic/knockoutmousemodelswithfattissue-selectiveinactivationofseveralkeyinflammatory
pathways,whicharecurrentlyundercomprehensivephenotypiccharacterization.