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dc.contributor.authorZaitune, Clarissa R.pt_BR
dc.contributor.authorFonseca, Tatiana de Lourdespt_BR
dc.contributor.authorCapelo, Luciane Portaspt_BR
dc.contributor.authorFreitas, Fatima Rodrigues de Sousa ept_BR
dc.contributor.authorBeber, Eduardo Henriquept_BR
dc.contributor.authorDora, José Miguel Silvapt_BR
dc.contributor.authorWang, Charles Chenweipt_BR
dc.contributor.authorRodrigues, Manuela Mirandapt_BR
dc.contributor.authorNonaka, Keico Okinopt_BR
dc.contributor.authorMaia, Ana Luiza Silvapt_BR
dc.contributor.authorGouveia, Cecilia H. A.pt_BR
dc.date.accessioned2020-12-11T04:12:17Zpt_BR
dc.date.issued2019pt_BR
dc.identifier.issn1664-2392pt_BR
dc.identifier.urihttp://hdl.handle.net/10183/216433pt_BR
dc.description.abstractC3H/HeJ (C3H) mice are deficient of type I deiodinase (D1), an enzyme that activates thyroid hormone (TH), converting thyroxine (T4) to triiodothyronine (T3). Nevertheless, C3H mice present normal serum T3 and a gross euthyroid phenotype. To investigate if a global D1 deficiency interferes in the TH effects on bone, we compared bone growth, bone mass accrual and bone strength of C3H and C57BL/6J (B6) mice under abnormal TH status. Four-week-old female mice of both strains were grouped as Euthyroid, Hypothyroid (pharmacologically-induced), 1xT4 and 10xT4 (hypothyroid animals receiving 1- or 10-fold the physiological dose of T4 /day/16 weeks). Hypothyroidism and TH excess similarly impaired body weight (BW) gain and body growth in both mice strains. In contrast, whereas hypothyroidism only slightly impaired bone mineral density (BMD) accrual in B6 mice, it severely impaired BMD accrual in C3H mice. No differences were observed in serum and bone concentrations of T3 between hypothyroid animals of both strains. Interestingly, treatment with 10xT4 was less deleterious to BMD accrual in C3H than in B6 mice and resulted in less elevated T3 serum levels in B6 than in C3H mice, which is probably explained by the lower D1 activity in C3H mice. In addition, hypothyroidism decreased bone strength only in C3H but not in B6 mice, while TH excess decreased this parameter in both strains. These findings indicate that D1 deficiency contributes to the TH excess-induced differences in bone mass accrual in C3H vs. B6 mice and suggest that deiodinase-unrelated genetic factors might account for the different skeleton responses to hypothyroidism between strains.en
dc.format.mimetypeapplication/pdfpt_BR
dc.language.isoengpt_BR
dc.relation.ispartofFrontiers in endocrinology. Lausanne. Vol. 10 (May 2019), 11 p.pt_BR
dc.rightsOpen Accessen
dc.subjectHormônios tireóideospt_BR
dc.subjectThyroid hormoneen
dc.subjectIodothyronine deiodinasesen
dc.subjectIodeto peroxidasept_BR
dc.subjectBone mass accrualen
dc.subjectDesenvolvimento ósseopt_BR
dc.subjectDensidade ósseapt_BR
dc.subjectBone growthen
dc.subjectC3H/HeJ and C57BL/6Jen
dc.subjectModelos animaispt_BR
dc.subjectCamundongos endogâmicos C3Hpt_BR
dc.titleAbnormal thyroid hormone status differentially affects bone mass accrual and bone strength in C3H/HeJ mice: a mouse model of type I deiodinase deficiencypt_BR
dc.typeArtigo de periódicopt_BR
dc.identifier.nrb001118634pt_BR
dc.type.originEstrangeiropt_BR


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