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血清脂肪因子水平升高与非肥胖类风湿关节炎女性的肌肉减少症有关。

Increased serum adipokines are associated with sarcopenia in non-obese women with rheumatoid arthritis.

机构信息

Graduate Institute of Clinical Medicine, College of Medicine, Kaohsiung Medical University, Taiwan.

Division of Geriatrics and Gerontology, Department of Internal Medicine, Kaohsiung Medical University Hospital, Taiwan.

出版信息

Kaohsiung J Med Sci. 2024 May;40(5):489-498. doi: 10.1002/kjm2.12823. Epub 2024 Apr 11.

Abstract

Large cohort studies have disclosed the association between obesity and rheumatoid arthritis (RA) risk. The sarcopenia prevalence in RA patients can be up to 31%. However, there is little information linking adipokines to sarcopenia in RA, so this study aimed to investigate whether adipokines were indeed involved in secondary sarcopenia in RA with a focus on non-obese females. Sixty-four female patients and 36 controls were included in this study. The serum adipokine levels (leptin and adiponectin) were determined by ELISA kits. The impacts of adipokines on muscle atrophy and potential autophagy were examined in mouse myoblasts, C2C12, upon treatment with recombinant leptin and adiponectin agonist (AdipoRan). Interestingly, serum adiponectin was significantly increased but the ratio of leptin/adiponectin was dramatically decreased in the RA patients with sarcopenia. After normalization by body mass, serum leptin was positively associated but adiponectin was negatively associated with muscle mass respectively, even after adjustment for fat mass. Treating C2C12 cells with leptin and AdipoRan inhibited proliferation of mature myotube respectively, as did treatment with the serum from RA patients. A combination of low leptin and high AdipoRan greatly decreased myogenin, but instead increased MAFbx and MuRF-1 as well as increased Beclin 1, Atg5, and LC3β. Taken together, our study reveals that secondary sarcopenia of RA females may be an imbalance of RA-related, but not obesity-related, increase in adipokine production; additionally, the reduced leptin/adiponectin ratio could be a better indicator in monitoring sarcopenia in non-obese RA females. Moreover, adipokine imbalance may promote muscle atrophy through inducing autophagy.

摘要

大型队列研究揭示了肥胖与类风湿关节炎(RA)风险之间的关联。RA 患者的肌少症患病率可高达 31%。然而,关于脂肪因子与 RA 肌少症的关系信息较少,因此本研究旨在探讨脂肪因子是否确实与非肥胖女性 RA 中的继发性肌少症有关。本研究纳入了 64 名女性患者和 36 名对照。通过 ELISA 试剂盒测定血清脂肪因子(瘦素和脂联素)水平。在使用重组瘦素和脂联素激动剂(AdipoRan)处理 C2C12 细胞后,检测脂肪因子对肌萎缩和潜在自噬的影响。有趣的是,RA 肌少症患者的血清脂联素水平显著升高,但瘦素/脂联素比值明显降低。经体重校正后,血清瘦素与肌肉量呈正相关,脂联素与肌肉量呈负相关,即使在调整体脂后也是如此。用瘦素和 AdipoRan 处理 C2C12 细胞分别抑制成熟肌管的增殖,RA 患者的血清处理也有同样的效果。低瘦素和高脂联素的组合大大降低了肌生成素,但增加了 MAFbx 和 MuRF-1,同时增加了 Beclin 1、Atg5 和 LC3β。总之,我们的研究表明,RA 女性的继发性肌少症可能是与 RA 相关而不是肥胖相关的脂肪因子产生增加的不平衡所致;此外,降低的瘦素/脂联素比值可能是监测非肥胖 RA 女性肌少症的更好指标。此外,脂肪因子失衡可能通过诱导自噬促进肌肉萎缩。

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