简介:Anovertphenotypeofaquaporin-1knockout(AQP1ko)miceisgrowthretardation,suggestingpossibledefectsinbonedevelopmentandmetabolism.Inthepresentstudy,weanalyzedthebonemineraldensity(BMD),bonecalciumandphosphoruscontents,andbonemetabolisminanAQP1komousemodel.TheBMDoffemursinAQP1komicewassignificantlylowerthanthatoflitter-matchedwildtypemiceasmeasuredbydualenergyX-rayabsorptiometry.Consistently,thecontentsofbonetotalcalciumandphosphoruswerealsosignificantlylowerinAQP1komice.ThereducedBMDcausedbyAQP1deficiencymainlyaffectmalemice.Bonemetabolicactivity,asindicatedby99mTc-MDPabsorptionmeasurements,wasremarkablyreducedinAQP1komice.TheseresultsprovidethefirstevidencethatAQP1playanimportantroleinbonestructureandmetabolism.