Excessive Food Intake, Obesity and Inflammation Process in Zucker fafa Rat Pancreatic Islets 英文参考文献.docVIP

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Excessive Food Intake, Obesity and Inflammation Process in Zucker fafa Rat Pancreatic Islets 英文参考文献.doc

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Excessive Food Intake, Obesity and Inflammation Process in Zucker fafa Rat Pancreatic Islets 英文参考文献

ExcessiveFoodIntake,ObesityandInflammationProcess inZuckerfa/faRatPancreaticIslets MyriamChentouf1,GregorDubois2,Ce′lineJahannaut1,Franc?oiseCastex1,AnneDominiqueLajoix1, Rene′ Gross1,SylviePeraldi-Roux1* 1Centre National de la Recherche Scientifique – Formation de Recherche en Evolution 3400, Centre de Pharmacologie et Innovation pour le Diabe`te, Faculte′ de Pharmacie,Montpellier,France,2InstitutdeRecherchepourleDe′veloppement, Unite′ MixtedeRecherche,Faculte′ dePharmacie,Montpellier,France Abstract Inappropriatefoodintake-relatedobesityandmoreimportantly,visceraladiposity,aremajorriskfactorsfortheonsetof type2diabetes.Evidenceisemergingthatnutriment-inducedb-celldysfunctioncouldberelatedtoindirectinductionofa state of low grade inflammation. Our aim was to study whether hyperphagia associated obesity could promote an inflammatory response in pancreatic islets leading to ?-cell dysfunction. In the hyperphagic obese insulin resistant male Zuckerrat,wemeasuredthelevelofcirculatingpro-inflammatorycytokinesandestimatedtheirproductionaswellasthe expression of their receptors in pancreatic tissue and b-cells. Our main findings concern intra-islet pro-inflammatory cytokinesfromfa/farats:IL-1b,IL-6andTNFaexpressionswereincreased;IL-1R1wasalsoover-expressedwithacellular redistributionalsoobservedforIL-6R.Togetinsightintothemechanismsinvolvedinphenotypicalterations,abArrayswere usedtodeterminetheexpressionprofileofproteinsimplicatedindifferentmembranereceptorssignaling,apoptosisand cell cycle pathways. Despite JNK overexpression, cell viability was unaffected probably because of decreases in cleaved caspase3aswellasinSMAC/DIABLOandAPP,involvedintheinductionandamplificationofapoptosis.Concerningb-cell proliferation, decreases in important cell cycle regulators (Cyclin D1, p35) and increased expression of SMAD4 probably contribute to counteract and restrain hyperplasia in fa/fa rat islets. Finally and probably as a result of IL-1b and IL-1R1 increased expressions with