ArticleJCI insight2023
Mitochondrial β-oxidation of adipose-derived fatty acids by osteoblasts fuels parathyroid hormone-induced bone formation.
Article in JCI insight, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 21 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
21 citing papers in PubMed, 28 citations in OpenAlex.
- Article
- Histone arginine demethylase JMJD7 promotes bone formation through regulating α-Ketoglutarate metabolism.Cell death and differentiation · 2026Article
- Sclerostin deficiency sensitizes white adipocytes to thermogenic signals that induce beiging in mice.Nature communications · 2026Article
- Article
- Unveiling Epigenetic Molecular Mechanisms in Bone Fracture Risk: Insights From 731 Immune Cells, 1400 Metabolites, and Critical Genetic Pathways.Mediators of inflammation · 2026Article
- Increased fatty acid availability improves the osteo-anabolic effects of intermittent parathyroid hormone (iPTH) in murine models.Bone reports · 2025Article
- The role of bone in whole-body energy metabolism.Nature reviews. Endocrinology · 2025Review
- Effects of Lipid Metabolites and Cross Organ Lipid Metabolism Regulation on Bone Homeostasis.Aging and disease · 2025Review
- Metabolic Rewiring and Post-Translational Modifications: Unlocking the Mechanisms of Bone Turnover in Osteoporosis.Aging and disease · 2025Review
- Repair mechanisms of bone system tissues based on comprehensive perspective of multi-omics.Cell biology and toxicology · 2025Review
- Enhanced fatty acid oxidation in osteoprogenitor cells provides protection from high-fat diet induced bone dysfunction.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2025Article
- Dual release scaffolds as a promising strategy for enhancing bone regeneration: an updated review.Nanomedicine (London, England) · 2025Review
- Trimethylamine-N-oxide accelerates osteoporosis by PERK activation of ATF5 unfolding.Cellular and molecular life sciences : CMLS · 2024Article
- PTH receptor signalling, osteocytes and bone disease induced by diabetes mellitus.Nature reviews. Endocrinology · 2024Review
- Preclinical Rodent Models for Human Bone Disease, Including a Focus on Cortical Bone.Endocrine reviews · 2024Review
- Metabolic regulation of skeletal cell fate and function.Nature reviews. Endocrinology · 2024Review
- Review
- NOX4-reactive oxygen species axis: critical regulators of bone health and metabolism.Frontiers in cell and developmental biology · 2024Review
- Diet-Stimulated Marrow Adiposity Fails to Worsen Early, Age-Related Bone Loss.Obesity facts · 2024Article
- The Multifaceted Roles of Bone Marrow Adipocytes in Bone and Hematopoietic Homeostasis.The Journal of clinical endocrinology and metabolism · 2023Review
Corrections and comments
- Erratum issued
Authors and funding
13 authors at 5 institutions in 1 country.
Funding
Abstract
The energetic costs of bone formation require osteoblasts to coordinate their activities with tissues, like adipose, that can supply energy-dense macronutrients. In the case of intermittent parathyroid hormone (PTH) treatment, a strategy used to reduce fracture risk, bone formation is preceded by a change in systemic lipid homeostasis. To investigate the requirement for fatty acid oxidation by osteoblasts during PTH-induced bone formation, we subjected mice with osteoblast-specific deficiency of mitochondrial long-chain β-oxidation as well as mice with adipocyte-specific deficiency for the PTH receptor or adipose triglyceride lipase to an anabolic treatment regimen. PTH increased the release of fatty acids from adipocytes and β-oxidation by osteoblasts, while the genetic mouse models were resistant to the hormone's anabolic effect. Collectively, these data suggest that PTH's anabolic actions require coordinated signaling between bone and adipose, wherein a lipolytic response liberates fatty acids that are oxidized by osteoblasts to fuel bone formation.
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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.