ArticleBiological procedures online2009
Streptozotocin, type I diabetes severity and bone.
Article in Biological procedures online, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 2 of them syntheses that pooled it.
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Who cites it
71 citing papers in PubMed, 2 syntheses or guidelines pooled it, 140 citations in OpenAlex.
- Liraglutide, a glucagon-like peptide-1 receptor agonist, inhibits bone loss in an animal model of osteoporosis with or without diabetes.Frontiers in endocrinology · 2024Pooled it
- Meta-analysis of Diabetes Mellitus-Associated Differences in Bone Structure Assessed by High-Resolution Peripheral Quantitative Computed Tomography.Current osteoporosis reports · 2022Pooled it
- Evaluation of the pro-healing effect of a commercial formulation of aqueous extract of Triticum vulgare in hyperglycemic miceBiomedica : revista del Instituto Nacional de Salud · 2026Article
- Evaluation of the anti-hyperglycemic and anti-dyslipidemic potential of the hydroethanolic extract ofMetabolism open · 2026Article
- Antihyperglycemic and pancreatic tissue-preserving effects ofFrontiers in endocrinology · 2026Article
- Pancreatic β-cell FFA2 deficiency suppresses multiple low dose streptozotocin induced diabetes in male mice.Communications biology · 2025Article
- Examination of Skeletal and Senescence Phenotypes in Young Mice with Juvenile Onset Type 1 Diabetes.Calcified tissue international · 2025Article
- Article
- Cross-tissue transcriptome-wide association identify novel T1D susceptibility genes and drug candidates.Frontiers in immunology · 2025Article
- Metformin attenuates diabetic osteoporosis by suppressing ferroptosis via the AMPK/Nrf2 pathway.Frontiers in pharmacology · 2025Article
- Synbiotic supplementation ameliorates anxiety and myocardial ischaemia-reperfusion injury in hyperglycaemic rats by modulating gut microbiota.Experimental physiology · 2024Article
- Longitudinal Analysis of Bone Metabolic Markers and Bone Mechanical Properties in STZ-Induced Diabetic Rats.Journal of clinical medicine · 2024Article
- Quercetin prevents kidney against diabetes mellitus (type 1) in rats by inhibiting TGF-β/apelin gene expression.Molecular biology reports · 2024Article
- Sarm1 knockout prevents type 1 diabetic bone disease in females independent of neuropathy.JCI insight · 2024Article
- Article
- Skeletal manifestations in a streptozotocin-induced C57BL/6 model of Type 1 diabetes.Bone reports · 2022Article
- Astaxanthin Protects against Hyperglycemia-Induced Oxidative and Inflammatory Damage to Bone Marrow and to Bone Marrow-Retained Stem Cells and Restores Normal Hematopoiesis in Streptozotocin-Induced Diabetic Mice.Antioxidants (Basel, Switzerland) · 2022Article
- Dysregulated transforming growth factor-beta mediates early bone marrow dysfunction in diabetes.Communications biology · 2022Article
- Article
- Preexisting Type 1 Diabetes Mellitus Blunts the Development of Posttraumatic Osteoarthritis.JBMR plus · 2022Article
11 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
As many as 50% of adults with type I (T1) diabetes exhibit bone loss and are at increased risk for fractures. Therapeutic development to prevent bone loss and/or restore lost bone in T1 diabetic patients requires knowledge of the molecular mechanisms accounting for the bone pathology. Because cell culture models alone cannot fully address the systemic/metabolic complexity of T1 diabetes, animal models are critical. A variety of models exist including spontaneous and pharmacologically induced T1 diabetic rodents. In this paper, we discuss the streptozotocin (STZ)-induced T1 diabetic mouse model and examine dose-dependent effects on disease severity and bone. Five daily injections of either 40 or 60 mg/kg STZ induce bone pathologies similar to spontaneously diabetic mouse and rat models and to human T1 diabetic bone pathology. Specifically, bone volume, mineral apposition rate, and osteocalcin serum and tibia messenger RNA levels are decreased. In contrast, bone marrow adiposity and aP2 expression are increased with either dose. However, high-dose STZ caused a more rapid elevation of blood glucose levels and a greater magnitude of change in body mass, fat pad mass, and bone gene expression (osteocalcin, aP2). An increase in cathepsin K and in the ratio of RANKL/OPG was noted in high-dose STZ mice, suggesting the possibility that severe diabetes could increase osteoclast activity, something not seen with lower doses. This may contribute to some of the disparity between existing studies regarding the role of osteoclasts in diabetic bone pathology. Examination of kidney and liver toxicity indicate that the high STZ dose causes some liver inflammation. In summary, the multiple low-dose STZ mouse model exhibits a similar bone phenotype to spontaneous models, has low toxicity, and serves as a useful tool for examining mechanisms of T1 diabetic bone loss.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.