Mitochondrial β-oxidation of adiposederived fatty acids by osteoblasts fuels parathyroid hormone-induced bone formation

Nathalie S. Alekos, Priyanka Kushwaha, Soohyun P. Kim, Zhu Li, Abdullah Abood, Naomi Dirckx, Susan Aja, Joe Kodama, Jean G. Garcia-Diaz, Satoru Otsuru, Elizabeth Rendina-Ruedy, Michael J. Wolfgang, Ryan C. Riddle

Research output: Contribution to journalArticlepeer-review

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 osteoblastspecific 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.

Original languageEnglish (US)
Article numbere165604
JournalJCI Insight
Volume8
Issue number6
DOIs
StatePublished - Mar 22 2023

ASJC Scopus subject areas

  • General Medicine

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