{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Hu P"],"funding":["OREF","NCATS NIH HHS","NCRR NIH HHS","NIDDK NIH HHS","NCI NIH HHS","NIH","NIAMS NIH HHS"],"pagination":["115906"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8546917"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["147"],"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"],"journal":["Bone"],"pubmed_title":["Type 1 diabetic Akita mice have low bone mass and impaired fracture healing."],"pmcid":["PMC8546917"],"funding_grant_id":["P30 AR074992","P30 CA091842","R21 AR066798","UL1 TR002345","P30 AR057235","P30 DK020579","S10 RR023660","R01 AR050211","S10 RR027552"],"pubmed_authors":["Migotsky N","Gardner MJ","Buettmann EG","McKenzie JA","Silva MJ","Hu P"],"additional_accession":[]},"is_claimable":false,"name":"Type 1 diabetic Akita mice have low bone mass and impaired fracture healing.","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","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Jun","modification":"2026-05-05T03:13:15.997Z","creation":"2025-04-19T18:17:55.096Z"},"accession":"S-EPMC8546917","cross_references":{"pubmed":["33662611"],"doi":["10.1016/j.bone.2021.115906"]}}