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Altered bone microarchitecture in a type 1 diabetes mouse model Ins2 (Akita)

2018Journal article Open access
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dc.contributor.authorPires De Carvalho, Filipe Ricardo
dc.contributor.authorCalado, Sofia
dc.contributor.authorSilva, Gabriela A.
dc.contributor.authorDiogo, Gabriela S.
dc.contributor.authorMoreira da Silva, Joana
dc.contributor.authorReis, Rui L.
dc.contributor.authorCancela, M. Leonor
dc.contributor.authorGavaia, Paulo
dc.date.accessioned2020-07-29T12:08:00Z
dc.date.available2020-07-29T12:08:00Z
dc.date.issued2018
dc.description.abstractType 1 diabetes mellitus (T1DM) has been associated to several cartilage and bone alterations including growth retardation, increased fracture risk, and bone loss. To determine the effect of long term diabetes on bone we used adult and aging Ins2 Akita mice that developed T1DM around 3-4 weeks after birth. Both Ins2 Akita and wild-type (WT) mice were analyzed at 4, 6, and 12 months to assess bone parameters such as femur length, growth plate thickness and number of mature and preapoptotic chondrocytes. In addition, bone microarchitecture of the cortical and trabecular regions was measured by microcomputed tomography and gene expression of Adamst-5, Col2, Igf1, Runx2, Acp5, and Oc was quantified by quantitative real-time polymerase chain reaction. Ins2 Akita mice showed a decreased longitudinal growth of the femur that was related to decreased growth plate thickness, lower number of chondrocytes and to a higher number of preapoptotic cells. These changes were associated with higher expression of Adamst-5, suggesting higher cartilage degradation, and with low expression levels of Igf1 and Col2 that reflect the decreased growth ability of diabetic mice. Ins2 Akita bone morphology was characterized by low cortical bone area (Ct.Ar) but higher trabecular bone volume (BV/TV) and expression analysis showed a downregulation of bone markers Acp5, Oc, and Runx2. Serum levels of insulin and leptin were found to be reduced at all-time points Ins2 Akita . We suggest that Ins2 Akita mice bone phenotype is caused by lower bone formation and even lower bone resorption due to insulin deficiency and to a possible relation with low leptin signaling.pt_PT
dc.description.sponsorshipSFRH/BD/76873/2011/ SFRH/BD/76429/2011/ PEst-C/MAR/LA0015/2011pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.doi10.1002/jcp.27617pt_PT
dc.identifier.issn0021-9541
dc.identifier.urihttp://hdl.handle.net/10400.1/14540
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherWileypt_PT
dc.relationDevelopment of new gene therapy approaches for the treatment of ocular neovascularization
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/pt_PT
dc.subjectAnimalspt_PT
dc.subjectApoptosispt_PT
dc.subjectBiomarkerspt_PT
dc.subjectBlood glucosept_PT
dc.subjectBody weightpt_PT
dc.subjectCancellous bonept_PT
dc.subjectCartilagept_PT
dc.subjectCortical bonept_PT
dc.subjectDiabetes mellituspt_PT
dc.subjectDisease modelspt_PT
dc.subjectFemurpt_PT
dc.subjectGene expression regulationpt_PT
dc.subjectGrowth platept_PT
dc.subjectInsulinpt_PT
dc.subjectLeptinpt_PT
dc.subjectMalept_PT
dc.subjectMicept_PT
dc.subjectOrgan sizept_PT
dc.subjectTartrate-resistant acid phosphatasept_PT
dc.subjectType 1pt_PT
dc.subjectInbred C57BLpt_PT
dc.subjectAnimalpt_PT
dc.titleAltered bone microarchitecture in a type 1 diabetes mouse model Ins2 (Akita)pt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.awardTitleDevelopment of new gene therapy approaches for the treatment of ocular neovascularization
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/SFRH/SFRH%2FBD%2F76429%2F2011/PT
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/5876/UID%2FMulti%2F04326%2F2013/PT
oaire.awardURIinfo:eu-repo/grantAgreement/EC/FP7/249314/EU
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/5876/UID%2FBIM%2F04773%2F2013/PT
oaire.citation.endPage9350pt_PT
oaire.citation.issue6pt_PT
oaire.citation.startPage9338pt_PT
oaire.citation.titleJournal of Cellular Physiologypt_PT
oaire.citation.volume234pt_PT
oaire.fundingStreamSFRH
oaire.fundingStream5876
oaire.fundingStreamFP7
oaire.fundingStream5876
person.familyNamePires de Carvalho
person.familyNameCalado
person.familyNameSilva
person.familyNameCancela
person.familyNameGavaia
person.givenNameFilipe Ricardo
person.givenNameSofia
person.givenNameGabriela
person.givenNameM. Leonor
person.givenNamePaulo
person.identifier.ciencia-id181A-A440-7D6E
person.identifier.ciencia-id7C1A-91BA-B6A0
person.identifier.ciencia-idDC1E-F164-FDD9
person.identifier.ciencia-idB619-FC16-D007
person.identifier.orcid0000-0002-1468-0305
person.identifier.orcid0000-0001-5509-4145
person.identifier.orcid0000-0001-5946-1918
person.identifier.orcid0000-0003-3114-6662
person.identifier.orcid0000-0002-9582-1957
person.identifier.ridK-2202-2016
person.identifier.ridF-4409-2012
person.identifier.ridA-6470-2011
person.identifier.scopus-author-id55115644400
person.identifier.scopus-author-id56426215600
person.identifier.scopus-author-id7101647767
person.identifier.scopus-author-id6507104377
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.identifierhttp://doi.org/10.13039/501100008530
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.nameFundação para a Ciência e a Tecnologia
project.funder.nameFundação para a Ciência e a Tecnologia
project.funder.nameEuropean Commission
project.funder.nameFundação para a Ciência e a Tecnologia
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT
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