趋化素介导运动诱导的糖尿病或高脂饮食小鼠骨微观结构和骨量的改善。

IF 3.8 3区 医学 Q2 CELL BIOLOGY
Xiaohan Yu , Xinyan Pan , Mei Huang , Xiaoye Lin , Xiaohui Wang
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引用次数: 0

摘要

阐明脂肪因子趋化素在2型糖尿病(DM)小鼠和高脂饮食(HFD)小鼠运动诱导的骨骼改善中的作用和机制。通过HFD+链脲佐菌素注射建立DM小鼠,在跑步前补充外源性趋化素,发现外源性趋化素逆转了6周运动诱导的DM小鼠松质骨参数的改善。而脂肪特异性趋化素敲除可改善HFD小鼠松质骨的微观结构和质量,进一步增强运动诱导的骨质改善,同时促进成骨,抑制破骨,表现为RANKL、M-CSF、Runx2、Osterix、OPG、ALP和CTSK的变化。这些结果表明,减少的趋化素有助于运动诱导的DM和HFD小鼠松质骨的微观结构和质量增强,并与促进成骨和破骨抑制有关,这有助于阐明趋化素对久坐和运动状态下代谢性疾病的骨重塑的影响。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Chemerin mediates exercise-induced improvements of bone microstructure and bone mass in diabetes or high fat diet mice
To clarify the roles and mechanisms of adipokine chemerin in exercise-induced bone improvements in type 2 diabetes mellitus (DM) mice and mice fed on high fat diet (HFD). DM mice were established by HFD + streptozotocin injection, exogenous chemerin was supplemented prior to running, and found that exogenous chemerin reversed 6-week exercise-induced improvements in cancellous bone parameters in DM mice. While adipose-specific chemerin knockout improved microstructure and mass of cancellous bone in HFD mice and further increased exercise-induced bone improvements, accompanied with promoted osteogenesis and inhibited osteoclasis represented as the changes of RANKL, M-CSF, Runx2, Osterix, OPG, ALP and CTSK. These results indicated that reduced chemerin contributed to exercise-induced enhancements in the microstructure and mass of cancellous bone in DM and HFD mice in association with osteogenesis promotion and osteoclasis inhibition, which is beneficial to clarify chemerin's impact on bone remodeling in metabolic diseases at sedentary and exercise states.
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来源期刊
Molecular and Cellular Endocrinology
Molecular and Cellular Endocrinology 医学-内分泌学与代谢
CiteScore
9.00
自引率
2.40%
发文量
174
审稿时长
42 days
期刊介绍: Molecular and Cellular Endocrinology was established in 1974 to meet the demand for integrated publication on all aspects related to the genetic and biochemical effects, synthesis and secretions of extracellular signals (hormones, neurotransmitters, etc.) and to the understanding of cellular regulatory mechanisms involved in hormonal control.
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