ArticleThe Journal of clinical investigation2012
Osteoblasts mediate the adverse effects of glucocorticoids on fuel metabolism.
Article in The Journal of clinical investigation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers.
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
93 citing papers in PubMed, 186 citations in OpenAlex.
- The effect of prednisolone ingestion and acute exercise on lipocalin-2 and its variants in young men: a pilot randomised crossover study.Scientific reports · 2025Trial
- The contribution of serum cortisone and glucocorticoid metabolites to detrimental bone health in patients receiving hydrocortisone therapy.BMC endocrine disorders · 2020Trial
- Glucose-loading reduces bone remodeling in women and osteoblast function in vitro.Physiological reports · 2016Trial
- Recent advances in glucocorticoid regulation of bone and the bone marrow niche: Genetic and pharmacological approaches to understand and prevent bone loss.Current opinion in endocrine and metabolic research · 2026Article
- Fucoxanthin Ameliorates Polycystic Ovary Syndrome by Coordinated Modulation of NF-κB and Nrf2 Signaling: Evidence from a DHEA-Induced Mouse Model.Reproductive sciences (Thousand Oaks, Calif.) · 2026Article
- Bone Organoids: A Novel Tool for Modeling and Managing Skeletal Disorders in Diabetes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- The role of bone in whole-body energy metabolism.Nature reviews. Endocrinology · 2025Review
- Two decades into the crosstalk between bone and energy metabolism.Nature reviews. Endocrinology · 2025Article
- Article
- Bone and muscle crosstalk in ageing and disease.Nature reviews. Endocrinology · 2025Review
- Consensus on the key characteristics of metabolism disruptors.Nature reviews. Endocrinology · 2025Review
- Emerging therapeutic approaches in graves' ophthalmopathy: an update on pharmacological interventions.Frontiers in immunology · 2025Review
- IL-18BP Therapy Ameliorates Reproductive and Metabolic Phenotypes in a PCOS Mouse Model by Relieving Inflammation, Fibrosis and Endoplasmic Reticulum Stress.Reproductive sciences (Thousand Oaks, Calif.) · 2024Article
- Targeting osteoblastic 11β-HSD1 to combat high-fat diet-induced bone loss and obesity.Nature communications · 2024Article
- Article
- Current knowledge of bone-derived factor osteocalcin: its role in the management and treatment of diabetes mellitus, osteoporosis, osteopetrosis and inflammatory joint diseases.Journal of molecular medicine (Berlin, Germany) · 2024Review
- Paradoxical improvement of dyspnoea in relapsing polychondritis by glucocorticoid tapering.BMJ case reports · 2024Article
- Endocrine Disorders and Peripheral Arterial Disease - A Series of Reviews Cushing Syndrome-Cortisol Excess.Current vascular pharmacology · 2024Review
- Management of Diabetes Mellitus in Acromegaly and Cushing's Disease with Focus on Pasireotide Therapy: A Narrative Review.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024Review
- Erythropoietin suppresses osteoblast apoptosis and ameliorates steroid-induced necrosis of the femoral head in rats by inhibition of STAT1-caspase 3 signaling pathway.BMC musculoskeletal disorders · 2023Article
33 more citing papers are in PubMed but not listed here.
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Authors and funding
14 authors at 5 institutions in 3 countries.
Funding
Abstract
Long-term glucocorticoid treatment is associated with numerous adverse outcomes, including weight gain, insulin resistance, and diabetes; however, the pathogenesis of these side effects remains obscure. Glucocorticoids also suppress osteoblast function, including osteocalcin synthesis. Osteocalcin is an osteoblast-specific peptide that is reported to be involved in normal murine fuel metabolism. We now demonstrate that osteoblasts play a pivotal role in the pathogenesis of glucocorticoid-induced dysmetabolism. Osteoblast-targeted disruption of glucocorticoid signaling significantly attenuated the suppression of osteocalcin synthesis and prevented the development of insulin resistance, glucose intolerance, and abnormal weight gain in corticosterone-treated mice. Nearly identical effects were observed in glucocorticoid-treated animals following heterotopic (hepatic) expression of both carboxylated and uncarboxylated osteocalcin through gene therapy, which additionally led to a reduction in hepatic lipid deposition and improved phosphorylation of the insulin receptor. These data suggest that the effects of exogenous high-dose glucocorticoids on insulin target tissues and systemic energy metabolism are mediated, at least in part, through the skeleton.
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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.