运动训练可减轻免疫介导坏死性肌病和皮肌炎患者骨骼肌脂肪浸润,改善胰岛素通路。

IF 1.1 4区 医学 Q4 Medicine Archives of rheumatology Pub Date : 2023-06-01 DOI:10.46497/ArchRheumatol.2023.9257
Diego Sales de Oliveira, Isabela Bruna Pires Borges, Suely Kazue Nagahashi Marie, Antonio Marcondes Lerario, Sueli Mieko Oba-Shinjo, Samuel Katsuyuki Shinjo
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引用次数: 0

摘要

目的:本研究旨在评估运动训练对全身自身免疫性肌病(SAMs)患者肌内脂质含量和胰岛素通路相关基因的影响。患者和方法:2016年1月至2019年5月,共7例皮肌炎(DM;男性3人,女性4人;平均年龄49.8±2.3岁;43 - 54岁),6例免疫介导坏死性肌病(IMNM;3男,3女;平均年龄:58.5±10.6岁;年龄范围46 - 74岁),对照组10人(CTRL组;男性4名,女性6名;平均年龄:48.7±3.9岁;年龄范围为41岁至56岁)。干预前后分别进行肌肉活检以评估肌内脂质含量。患者接受了为期12周的联合运动训练计划。分析骨骼肌基因表达,比较DM组与对照组、DM干预前后、IMNM干预前后的差异。结果:DM组II型肌纤维肌内脂质含量高于对照组。干预后,DM组和IMNM组ⅰ型和ⅱ型纤维脂质含量降低。与DM组相比,CTRL组胰岛素和脂质氧化途径相关基因(AMPKβ2、AS160、INSR、PGC1-α、PI3K和RAB14)的表达显著增加。运动训练后,DM组(AMPKβ2、AS160、INSR、PGC1-α、PI3K、RAB14)和IMNM组(AKT2、AMPKβ2、RAB10、RAB14、PGC1-α)胰岛素通路和脂质氧化相关基因表达增加。结论:运动训练降低了糖尿病和IMNM患者I型和II型肌纤维中的脂肪量,增加了糖尿病和IMNM中胰岛素通路和脂质氧化相关基因的表达。这些结果表明,运动训练可以改善这些疾病骨骼肌的质量和代谢功能。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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Exercise training attenuates skeletal muscle fat infiltration and improves insulin pathway of patients with immune-mediated necrotizing myopathies and dermatomyositis.

Objectives: This study aims to evaluate the effects of exercise training on intramuscular lipid content and genes related to insulin pathway in patients with systemic autoimmune myopathies (SAMs).

Patients and methods: Between January 2016 and May 2019, a total of seven patients with dermatomyositis (DM; 3 males, 4 females; mean age: 49.8±2.3 years; range, 43 to 54 years), six with immune mediated necrotizing myopathy (IMNM; 3 males, 3 females; mean age: 58.5±10.6 years; range, 46 to 74 years), and 10 control individuals (CTRL group; 4 males, 6 females; mean age: 48.7±3.9 years; range, 41 to 56 years) were included. The muscle biopsy before and after the intervention was performed to evaluate the intramuscular lipid content. Patients underwent a combined exercise training program for 12 weeks. Skeletal muscle gene expression was analyzed and the DM versus CTRL group, DM pre- and post-, and IMNM pre- and post-intervention were compared.

Results: The DM group had a higher intramuscular lipid content in type II muscle fibers compared to the CTRL group. After the intervention, there was a reduction of lipid content in type I and II fibers in DM and IMNM group. The CTRL group showed a significantly higher expression of genes related to insulin and lipid oxidation pathways (AMPKβ2, AS160, INSR, PGC1-α, PI3K, and RAB14) compared to the DM group. After exercise training, there was an increase gene expression related to insulin pathway and lipid oxidation in DM group (AMPKβ2, AS160, INSR, PGC1-α, PI3K, and RAB14) and in IMNM group (AKT2, AMPKβ2, RAB10, RAB14, and PGC1-α).

Conclusion: Exercise training attenuated the amount of fat in type I and II muscle fibers in patients with DM and IMNM and increased gene expression related to insulin pathways and lipid oxidation in DM and IMNM. These results suggest that exercise training can improve the quality and metabolic functions of skeletal muscle in these diseases.

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来源期刊
Archives of rheumatology
Archives of rheumatology Medicine-Rheumatology
CiteScore
2.00
自引率
9.10%
发文量
15
期刊介绍: The Archives of Rheumatology is an official journal of the Turkish League Against Rheumatism (TLAR) and is published quarterly in March, June, September, and December. It publishes original work on all aspects of rheumatology and disorders of the musculoskeletal system. The priority of the Archives of Rheumatology is to publish high-quality original research articles, especially in inflammatory rheumatic disorders. In addition to research articles, brief reports, reviews, editorials, letters to the editor can also be published. It is an independent peer-reviewed international journal printed in English. Manuscripts are refereed by a "double-blind peer-reviewed" process for both referees and authors. Editorial Board of the Archives of Rheumatology works under the principles of The World Association of Medical Editors (WAME), the International Council of Medical Journal Editors (ICMJE), and Committee on Publication Ethics (COPE).
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