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Corrigendum Open Access | 10.1172/jci.insight.198337

Mitochondrial β-oxidation of adipose-derived 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, and Ryan C. Riddle

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Published September 23, 2025 - More info

Published in Volume 10, Issue 18 on September 23, 2025
JCI Insight. 2025;10(18):e198337. https://doi.org/10.1172/jci.insight.198337.
© 2025 Alekos et al. This work is licensed under the Creative Commons Attribution 4.0 International License. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
Published September 23, 2025 - Version history
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Mitochondrial β-oxidation of adipose-derived 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
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 Article Bone biology

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

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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.

Authors

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

×

Original citation: JCI Insight. 2023;8(6):e165604. https://doi.org/10.1172/jci.insight.165604

Citation for this corrigendum: JCI Insight. 2025;10(18):e198337. https://doi.org/10.1172/jci.insight.198337

The authors recently became aware that in Figure 6D, the AdΔAtgl panel was inadvertently duplicated from the control panel during the revision process. The correct panel is provided below. The HTML and PDF files have been updated.

Figure 6

The authors regret the error.

Footnotes

See the related article at Mitochondrial β-oxidation of adipose-derived fatty acids by osteoblasts fuels parathyroid hormone–induced bone formation.

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