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Publication : Mitochondrial β-oxidation of adipose-derived fatty acids by osteoblasts fuels parathyroid hormone-induced bone formation.

First Author  Alekos NS Year  2023
Journal  JCI Insight Volume  8
Issue  6 PubMed ID  36729662
Mgi Jnum  J:353045 Mgi Id  MGI:7460692
Doi  10.1172/jci.insight.165604 Citation  Alekos NS, et al. (2023) Mitochondrial beta-oxidation of adipose-derived fatty acids by osteoblasts fuels parathyroid hormone-induced bone formation. JCI Insight 8(6)
abstractText  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 beta-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 beta-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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