<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Hu P</submitter><funding>OREF</funding><funding>NCATS NIH HHS</funding><funding>NCRR NIH HHS</funding><funding>NIDDK NIH HHS</funding><funding>NCI NIH HHS</funding><funding>NIH</funding><funding>NIAMS NIH HHS</funding><pagination>115906</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8546917</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>147</volume><pubmed_abstract>Type 1 diabetes (T1DM) impairs bone formation and fracture healing in humans. Akita mice carry a mutation in one allele of the insulin-2 (Ins2) gene, which leads to pancreatic beta cell dysfunction and hyperglycemia by 5-6 weeks age. We hypothesized that T1DM in Akita mice is associated with decreased bone mass, weaker bones, and impaired fracture healing. Ins2 ± (Akita) and wildtype (WT) males were subjected to femur fracture at 18-weeks age and healing assessed 3-21 days post-fracture. Non-fractured left femurs were assessed for morphology (microCT) and strength (bending or torsion) at 19-21 weeks age. Fractured right femurs were assessed for callus mechanics (torsion), morphology and composition (microCT and histology) and gene expression (qPCR). Both Akita and WT mice gained weight fro</pubmed_abstract><journal>Bone</journal><pubmed_title>Type 1 diabetic Akita mice have low bone mass and impaired fracture healing.</pubmed_title><pmcid>PMC8546917</pmcid><funding_grant_id>P30 AR074992</funding_grant_id><funding_grant_id>P30 CA091842</funding_grant_id><funding_grant_id>R21 AR066798</funding_grant_id><funding_grant_id>UL1 TR002345</funding_grant_id><funding_grant_id>P30 AR057235</funding_grant_id><funding_grant_id>P30 DK020579</funding_grant_id><funding_grant_id>S10 RR023660</funding_grant_id><funding_grant_id>R01 AR050211</funding_grant_id><funding_grant_id>S10 RR027552</funding_grant_id><pubmed_authors>Migotsky N</pubmed_authors><pubmed_authors>Gardner MJ</pubmed_authors><pubmed_authors>Buettmann EG</pubmed_authors><pubmed_authors>McKenzie JA</pubmed_authors><pubmed_authors>Silva MJ</pubmed_authors><pubmed_authors>Hu P</pubmed_authors></additional><is_claimable>false</is_claimable><name>Type 1 diabetic Akita mice have low bone mass and impaired fracture healing.</name><description>Type 1 diabetes (T1DM) impairs bone formation and fracture healing in humans. Akita mice carry a mutation in one allele of the insulin-2 (Ins2) gene, which leads to pancreatic beta cell dysfunction and hyperglycemia by 5-6 weeks age. We hypothesized that T1DM in Akita mice is associated with decreased bone mass, weaker bones, and impaired fracture healing. Ins2 ± (Akita) and wildtype (WT) males were subjected to femur fracture at 18-weeks age and healing assessed 3-21 days post-fracture. Non-fractured left femurs were assessed for morphology (microCT) and strength (bending or torsion) at 19-21 weeks age. Fractured right femurs were assessed for callus mechanics (torsion), morphology and composition (microCT and histology) and gene expression (qPCR). Both Akita and WT mice gained weight fro</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Jun</publication><modification>2026-05-05T03:13:15.997Z</modification><creation>2025-04-19T18:17:55.096Z</creation></dates><accession>S-EPMC8546917</accession><cross_references><pubmed>33662611</pubmed><doi>10.1016/j.bone.2021.115906</doi></cross_references></HashMap>