The complex pathophysiology of bone fragility in obesity and type 2 diabetes mellitus: therapeutic targets to promote osteogenesis.
The complex pathophysiology of bone fragility in obesity and type 2 diabetes mellitus: therapeutic targets to promote osteogenesis.
复制标题
肥胖和2型糖尿病骨脆性的复杂病理生理学：促进成骨的治疗靶点。
DOI：
10.3389/fendo.2023.1168687
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发表时间：
2023
影响因子：
5.2
通讯作者：
中科院分区：
文献类型：
--
作者：
在日益肥胖和老龄化的人口中，与2型糖尿病(T2 DM)相关的骨折是主要的公共卫生问题。肥胖或2型糖尿病患者的骨密度正常或高于正常，但骨折的风险增加。因此，了解T2 DM和肥胖如何导致骨生理改变导致骨折风险增加的病理生理学和机制是至关重要的。虽然在这些患者中已经报道了增强的破骨细胞介导的骨吸收，但在T2 DM患者中最值得注意的是，由于成骨细胞分化和存活功能障碍，骨形成减少。研究表明，肥胖和T2 DM与脂肪生成增加有关，考虑到脂肪细胞、成骨细胞和成肌细胞起源于同一祖细胞，脂肪生成和肌肉生成最有可能是以减少成骨和肌肉生成为代价的。此外，新出现的数据表明，骨骼和代谢动态平衡之间存在相互关系，这表明这些生理过程可能受到共同的调控途径的控制。因此，本综述旨在探讨肥胖症和2型糖尿病患者骨系分化的复杂机制及其对骨病理生理学的影响，同时检查潜在的新的药理靶点或重新评估现有的改善骨内稳态的药物。
Fractures associated with Type2 diabetes (T2DM) are major public health concerns in an increasingly obese and aging population. Patients with obesity or T2DM have normal or better than normal bone mineral density but at an increased risk for fractures. Hence it is crucial to understand the pathophysiology and mechanism of how T2DM and obesity result in altered bone physiology leading to increased fracture risk. Although enhanced osteoclast mediated bone resorption has been reported for these patients, the most notable observation among patients with T2DM is the reduction in bone formation from mostly dysfunction in osteoblast differentiation and survival. Studies have shown that obesity and T2DM are associated with increased adipogenesis which is most likely at the expense of reduced osteogenesis and myogenesis considering that adipocytes, osteoblasts, and myoblasts originate from the same progenitor cells. Furthermore, emerging data point to an inter-relationship between bone and metabolic homeostasis suggesting that these physiologic processes could be under the control of common regulatory pathways. Thus, this review aims to explore the complex mechanisms involved in lineage differentiation and their effect on bone pathophysiology in patients with obesity and T2DM along with an examination of potential novel pharmacological targets or a re-evaluation of existing drugs to improve bone homeostasis.
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影响因子：
2.2
作者：
Sylvawani M;Setyohadi B;Purnamasari D;Abdullah M;Kurniawan MR
通讯作者：
Kurniawan MR
影响因子：
4.2
作者：
Wang Y;Grainger DW
通讯作者：
Grainger DW
影响因子：
4.1
作者：
Colleluori G;Aguirre L;Dorin R;Robbins D;Blevins D;Barnouin Y;Chen R;Qualls C;Villareal DT;Armamento-Villareal R
通讯作者：
Armamento-Villareal R
体重指数较高的性交男性的骨密度更高，骨质质量更好，但肌肉密度降低。
影响因子：
4.2
作者：
Aguirre LE;Colleluori G;Dorin R;Robbins D;Chen R;Jiang B;Qualls C;Villareal DT;Armamento-Villareal R
通讯作者：
Armamento-Villareal R
影响因子：
5.6
作者：
Xu R;Zeng Q;Xia C;Chen J;Wang P;Zhao S;Yuan W;Lou Z;Lin H;Xia H;Lv S;Xu T;Tong P;Gu M;Jin H
通讯作者：
Jin H