内科学
内分泌学
合成代谢
化学
甲状旁腺激素
脂肪组织
脂肪甘油三酯脂肪酶
脂肪细胞
成骨细胞
β氧化
激素敏感脂肪酶
脂肪酸
脂解
生物化学
生物
医学
钙
体外
作者
Nathalie Alekos,Priyanka Kushwaha,Soohyun Kim,Li Zhu,Abdullah Abood,Naomi Dirckx,Susan Aja,Joe Kodama,Jean Garcia-Diaz,Satoru Otsuru,Elizabeth Rendina-Ruedy,Michael J. Wolfgang,Ryan C. Riddle
出处
期刊:JCI insight
[American Society for Clinical Investigation]
日期:2023-03-22
卷期号:8 (6)
被引量:3
标识
DOI:10.1172/jci.insight.165604
摘要
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.
科研通智能强力驱动
Strongly Powered by AbleSci AI