Metabolic Impact of Adult-Onset, Isolated, Growth Hormone Deficiency (AOiGHD) Due to Destruction of Pituitary Somatotropes 英文参考文献.docVIP

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Metabolic Impact of Adult-Onset, Isolated, Growth Hormone Deficiency (AOiGHD) Due to Destruction of Pituitary Somatotropes 英文参考文献.doc

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Metabolic Impact of Adult-Onset, Isolated, Growth Hormone Deficiency (AOiGHD) Due to Destruction of Pituitary Somatotropes 英文参考文献

MetabolicImpactofAdult-Onset,Isolated,Growth HormoneDeficiency(AOiGHD)DuetoDestructionof PituitarySomatotropes RaulM.Luque1,2,3,QingLin1,2,Jose′ Co′rdoba-Chaco′n3,PapasaniV.Subbaiah2,ThorstenBuch4 ,Ari Waisman5,HugoVankelecom6,RhondaD.Kineman1,2* 1Research and Development Division, Jesse Brown VeteransAffairs Medical Center, Chicago, Illinois, United States of America, 2Department of Medicine, Section of Endocrinology, Diabetes and Metabolism, University of Illinois at Chicago, Chicago, Illinois, United States of America, 3Department of Cell Biology, Physiology and Immunology, University of Co′rdoba, Instituto Maimo′nides de Investigacio′n Biome′dica de Co′rdoba (IMIBIC), and CIBER Fisiopatolog?′a de la Obesidad y Nutricio′n (CIBERobn), Co′rdoba, Spain, 4Neuroimmunology Division, Institute of Experimental Immunology, Department of Pathology, University Hospital Zu¨rich, Zu¨rich, Switzerland,5InstituteforMolecularBiology,UniversityMedicalCentre,UniversityofMainz,Mainz,Germany,6LaboratoryofTissuePlasticity,DepartmentofMolecular CellBiology,UniversityofLeuven(K.U.Leuven),Leuven,Belgium Abstract Growthhormone(GH)inhibitsfataccumulationandpromotesproteinaccretion,thereforethefallinGHobservedwithweight gainandnormalagingmaycontributetometabolicdysfunction.Todirectlytestthishypothesisanovelmousemodelofadult onset-isolatedGHdeficiency(AOiGHD)wasgeneratedbycrossbreedingratGHpromoter-drivenCrerecombinasemice(Cre) withinduciblediphtheriatoxinreceptormice(iDTR)andtreatingadultCre+/2 ,iDTR +/2 offspringwithDTtoselectivelydestroy thesomatotropepopulationoftheanteriorpituitarygland,leadingtoareductionincirculatingGHandIGF-Ilevels.DT-treated +/2 Cre2/2 ,iDTR micewereusedasGH-intactcontrols.AOiGHDimprovedwholebodyinsulinsensitivityinbothlow-fatand high-fat fed mice. Consistent with improved insulin sensitivity, indirect calorimetry revealed AOiGHD mice preferentially utilizedcarbohydratesforenergymetabolism,ascomparedtoGH-intactcontrols.Inhigh-fat,butnotlow-fatfedAOiGHD mice,fa