Liang Chuanjie, Guo Yan, Liu Yongliang, Wang Yangjunjie, Xiao Jing, Li Haiying, Xiang Xinxin
Center of Translational Medicine, Zibo Central Hospital, Zibo, 255000, Shandong, China.
Department of Nuclear Medicine and Radiotherapy, Zibo Central Hospital, Zibo, 255000, Shandong, China.
Eur J Med Res. 2025 Aug 13;30(1):741. doi: 10.1186/s40001-025-02954-0.
Obesity-related osteoporosis is a metabolic disorder of the adipose tissue and bone caused by energy accumulation. The role of adipogenic and osteogenic differentiation and phenotypic transformation in the pathogenesis of osteoporosis and the relevant signaling mechanism are still unclear.
Obesity-related osteoporotic mice were generated. Oil Red O and von Kossa staining, RT-PCR, and Western blotting were used to detect the differentiation capability of bone marrow mesenchymal stem cells (BMSCs) and the changes in related signaling pathways.
High-energy states increased bone loss in ovariectomized mice, increased adipogenic differentiation, and inhibited the osteogenic differentiation of BMSCs from ovariectomized mice fed with a high-fat diet compared with those fed with a normal chow diet. The mTOR signaling pathway was activated during the adipogenic differentiation, while it did not change during the osteogenic differentiation of BMSCs from the ovariectomized group fed with a high-fat diet compared with the normal chow diet group. In vitro experiments showed that higher extracellular energy levels promoted adipogenic differentiation and inhibited osteogenic differentiation, while energy deficiency decreased adipogenic differentiation in mouse BMSCs through the mTOR signaling pathway.
The mTOR signaling pathway can mediate the phenotypic transformation of adipocytes and osteocytes in obesity-related osteoporotic mice.
肥胖相关骨质疏松症是一种由能量蓄积引起的脂肪组织和骨骼的代谢紊乱。成脂和成骨分化及表型转化在骨质疏松症发病机制中的作用以及相关信号机制仍不清楚。
构建肥胖相关骨质疏松症小鼠模型。采用油红O和冯库萨染色、逆转录-聚合酶链反应（RT-PCR）及蛋白质免疫印迹法检测骨髓间充质干细胞（BMSCs）的分化能力及相关信号通路的变化。
与正常饮食喂养的去卵巢小鼠相比，高能状态增加了去卵巢小鼠的骨质流失，增加了成脂分化，并抑制了高脂饮食喂养的去卵巢小鼠BMSCs的成骨分化。在成脂分化过程中，mTOR信号通路被激活，而与正常饮食组相比，高脂饮食喂养的去卵巢组BMSCs在成骨分化过程中该信号通路没有变化。体外实验表明，较高的细胞外能量水平促进成脂分化并抑制成骨分化，而能量缺乏通过mTOR信号通路降低小鼠BMSCs的成脂分化。
mTOR信号通路可介导肥胖相关骨质疏松症小鼠脂肪细胞和骨细胞的表型转化。
