瘦素抵抗与骨质疏松:代谢失衡中的骨健康调控机制
Leptin resistance and osteoporosis: mechanisms for regulating bone health in metabolic imbalances
  
DOI:10.3969/j.issn.1006-7108.2025.07.018
中文关键词:  瘦素  瘦素抵抗  骨质疏松  调控机制
英文关键词:leptin  leptin resistance  osteoporosis  regulatory mechanisms
基金项目:国家自然科学基金(81973878);南中医自然基金项目(XZR2020082);江苏省中医退行性骨关节病临床医学创新中心项目(2021040501);2021无锡市中医药管理局项目(ZYKJ202110)
作者单位
程霜1 尹恒1,2 胡卓仪2 吴世祥1 马勇1 郭杨1 张亚峰1,2* 1.南京中医药大学江苏 南京 210023 2.南京中医药大学附属无锡医院江苏 无锡 214071 
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中文摘要:
      瘦素是一种由脂肪组织分泌的激素,广泛参与能量平衡、免疫调节和骨代谢等生理过程。近年来,瘦素抵抗作为肥胖、代谢综合征等疾病的重要特征,逐渐被发现与骨质疏松的发生密切相关。瘦素抵抗导致瘦素信号传导的功能减弱,削弱了其对骨形成的促进作用,同时增加了骨吸收,加速了骨质疏松的进展。本文综述了瘦素抵抗通过直接调控JAK-STAT和PI3K/Akt/mTOR信号通路,间接影响交感神经系统、炎症免疫反应、内质网应激、线粒体功能、自噬及与其他激素相互作用的机制,探讨瘦素抵抗在骨代谢失衡中的多方面作用,在通过深入理解瘦素抵抗在骨代谢中具体作用的情况下,有望为骨质疏松的预防和治疗提供新的策略,尤其是针对于肥胖相关的骨质疏松患者。
英文摘要:
      Leptin is a hormone secreted by adipose tissue, widely involved in physiological processes such as energy balance, immune regulation, and bone metabolism. In recent years, leptin resistance, a hallmark of diseases like obesity and metabolic syndrome, has been increasingly recognized to be closely associated with the occurrence of osteoporosis. Leptin resistance leads to impaired leptin signaling, weakening its role in promoting bone formation while increasing bone resorption, thereby accelerating the progression of osteoporosis. This article reviews the mechanisms by which leptin resistance directly regulates the JAK-STAT and PI3K/Akt/mTOR signaling pathways, and indirectly affects the sympathetic nervous system, inflammation and immune responses, endoplasmic reticulum stress, mitochondrial function, autophagy, and interactions with other hormones. By exploring the multifaceted role of leptin resistance in bone metabolism imbalance, a deeper understanding of its specific effects in bone metabolism may offer new strategies for the prevention and treatment of osteoporosis, particularly in patients with obesity-related osteoporosis.
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