ArticleBone2013
Osteo-promoting effects of insulin-like growth factor I (IGF-I) in a mouse model of type 1 diabetes.
Article in Bone, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.
- An update on the role of RANKL-RANK/osteoprotegerin and WNT-ß-catenin signaling pathways in pediatric diseases.World journal of pediatrics : WJP · 2019Pooled it
- LNGFR promoting osteogenic differentiation of ectomesenchyme stem cells via activation of GHR-JAK-STAT/IGF1 signaling pathway.Stem cell research & therapy · 2026Article
- Effect of Canagliflozin Pretreatment on the Efficacy of Insulin Therapy to Rescue Type 1 Diabetes-Related Bone Fragility in Male Mice.Calcified tissue international · 2026Article
- Morroniside Improves Diabetic Osteoporosis via the AGE/RAGE/Wnt/β-Catenin Signaling Pathway.The Kaohsiung journal of medical sciences · 2025Article
- Examination of Skeletal and Senescence Phenotypes in Young Mice with Juvenile Onset Type 1 Diabetes.Calcified tissue international · 2025Article
- An Inexpensive 3D Printed Mouse Model of Successful, Complication-free Long Bone Distraction Osteogenesis.Plastic and reconstructive surgery. Global open · 2023Article
- Article
- Identification of the key exosomal lncRNAs/mRNAs in the serum during distraction osteogenesis.Journal of orthopaedic surgery and research · 2022Article
- High-Throughput Sequencing Reveals CXCR4 and IGF1 Behave Different Roles in Weightlessness Osteoporosis.Stem cells international · 2022Article
- Pathophysiology and treatment of osteoporosis: challenges for clinical practice in older people.Aging clinical and experimental research · 2021Review
- Sclerostin antibody treatment improves fracture outcomes in a Type I diabetic mouse model.Bone · 2016Article
- Type 1 diabetes patients have lower strength in femoral bone determined by quantitative computed tomography: A cross-sectional study.Journal of diabetes investigation · 2015Article
- Type 1 diabetes is associated with an increased risk of fracture across the life span: a population-based cohort study using The Health Improvement Network (THIN).Diabetes care · 2015Article
- Effects of sequentially released BMP-2 and BMP-7 from PELA microcapsule-based scaffolds on the bone regeneration.American journal of translational research · 2015Article
- IGF-1R/β-catenin signaling axis is involved in type 2 diabetic osteoporosis.Journal of Zhejiang University. Science. BArticle
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
objectiveUsing a streptozotocin (STZ)-induced mouse model of type 1 diabetes (T1D), we have previously demonstrated that long-term diabetes inhibits regenerative bone formation during tibial distraction osteogenesis (DO) and perturbs skeletal integrity by decreasing cortical thickness, bone mineral density and bone's resistance to fracture. Because long-standing T1D is also associated with a deficiency of insulin-like growth factor I (IGF-I), we examined the effects of systemic IGF-I treatment on skeletal microarchitecture and strength, as well as on bone formation in diabetic mice. RESEARCH DESIGN AND
methodsStreptozotocin-induced diabetic or control mice were treated with recombinant human IGF-I (rhIGF-I, 1.5mg/kg/day as subcutaneous infusion) or vehicle throughout a 14day DO procedure. Thereafter, trunk blood was assayed for glucose, insulin, rhIGF-I, mouse IGF-I and leptin. Bone formation in distracted tibiae was quantified. Effects on cortical bone strength and trabecular bone architecture were assessed by μCT analysis and three-point bend testing of contralateral femurs.
resultsNew bone formation during DO was reduced in diabetic mice but significantly improved with rhIGF-I treatment. The contralateral femurs of diabetic mice demonstrated significant reductions in trabecular thickness, yield strength and peak force of cortical bone, which were improved with rhIGF-I treatment. rhIGF-I also reduced intracortical porosity in control mice. However, treatment with rhIGF-I did not normalize serum glucose, or correct concurrent deficiencies of insulin or leptin seen in diabetes.
conclusionsThese findings demonstrate that despite persistent hyperglycemia, rhIGF-I promoted new bone formation and improved biomechanical properties of bone in a model of T1D, suggesting that it may be useful as a fracture preventative in this disease.
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Registered trials
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