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10.1172/jci.insight.198337
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Published September 23, 2025 - More info
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.
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.
The authors regret the error.