ArticleCalcified tissue international2012
Rosiglitazone inhibits bone regeneration and causes significant accumulation of fat at sites of new bone formation.
Article in Calcified tissue international, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
19 citing papers in PubMed, 47 citations in OpenAlex.
- Function and Regulation of Bone Marrow Adipose Tissue in Health and Disease: State of the Field and Clinical Considerations.Comprehensive Physiology · 2024Review
- DNA methylation analysis identifies key transcription factors involved in mesenchymal stem cell osteogenic differentiation.Biological research · 2023Article
- Osteocytes contributeFrontiers in endocrinology · 2023Article
- Diabetes and Impaired Fracture Healing: A Narrative Review of Recent Literature.Current osteoporosis reports · 2022Review
- Pharmacological Inhibition of Inositol Hexakisphosphate Kinase 1 Protects Mice against Obesity-Induced Bone Loss.Biology · 2022Article
- Nonenzymatic and Trophic Activities of Carboxypeptidase E Regulate Bone Mass and Bioenergetics of Skeletal Stem Cells in Mice.JBMR plus · 2020Article
- Combating osteoporosis and obesity with exercise: leveraging cell mechanosensitivity.Nature reviews. Endocrinology · 2019Review
- The Unique Metabolic Characteristics of Bone Marrow Adipose Tissue.Frontiers in endocrinology · 2019Review
- Stem cell therapy for enhancement of bone consolidation in distraction osteogenesis: A contemporary review of experimental studies.Bone & joint research · 2017Article
- Marrow Adipose Tissue: Skeletal Location, Sexual Dimorphism, and Response to Sex Steroid Deficiency.Frontiers in endocrinology · 2017Article
- The biology of bone lengthening.Journal of children's orthopaedics · 2016Review
- Protein Phosphatase PP5 Controls Bone Mass and the Negative Effects of Rosiglitazone on Bone through Reciprocal Regulation of PPARγ (Peroxisome Proliferator-activated Receptor γ) and RUNX2 (Runt-related Transcription Factor 2).The Journal of biological chemistry · 2016Article
- Exercise Regulation of Marrow Adipose Tissue.Frontiers in endocrinology · 2016Review
- Exercise Regulation of Marrow Fat in the Setting of PPARγ Agonist Treatment in Female C57BL/6 Mice.Endocrinology · 2015Article
- Partial agonist, telmisartan, maintains PPARγ serine 112 phosphorylation, and does not affect osteoblast differentiation and bone mass.PloS one · 2014Article
- Protein kinase inhibitor γ reciprocally regulates osteoblast and adipocyte differentiation by downregulating leukemia inhibitory factor.Stem cells (Dayton, Ohio) · 2013Article
- Article
- Inducible brown adipose tissue, or beige fat, is anabolic for the skeleton.Endocrinology · 2013Article
- The future of thiazolidinedione therapy in the management of type 2 diabetes mellitus.Current diabetes reports · 2013Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Thiazolidinediones (TZDs), peroxisome proliferator-activated receptor gamma activators, and insulin sensitizers represent drugs used to treat hyperglycemia in diabetic patients. Type 2 diabetes mellitus (T2DM) is associated with a twofold increase in fracture risk, and TZDs use increases this risk by an additional twofold. In this study, we analyzed the effect of systemic administration of the TZD rosiglitazone on new bone formation in two in vivo models of bone repair, a model of drilled bone defect regeneration (BDR) and distraction osteogenesis (DO) and a model of extended bone formation. Rosiglitazone significantly inhibited new endosteal bone formation in both models. This effect was correlated with a significant accumulation of fat cells, specifically at sites of bone regeneration. The diminished bone regeneration in the DO model in rosiglitazone-treated animals was associated with a significant decrease in cell proliferation measured by the number of cells expressing proliferating cell nuclear antigen and neovascularization measured by both the number of vascular sinusoids and the number of cells producing proangiogenic vascular endothelial growth factor at the DO site. In summary, rosiglitazone decreased new bone formation in both BDR and DO models of bone repair by mechanisms which include both intrinsic changes in mesenchymal stem cell proliferation and differentiation and changes in the local environment supporting angiogenesis and new bone formation. These studies suggest that bone regeneration may be significantly compromised in T2DM patients on TZD therapy.
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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.