Restoring skeletal muscle mass as an independent determinant of liver fat deposition improvement in MAFLD

IF 5.3 2区医学 Q2 CELL BIOLOGY

Skeletal Muscle Pub Date : 2023-12-19 DOI:10.1186/s13395-023-00333-z

Ting Zhou, Junzhao Ye, Ling Luo, Wei Wang, Shiting Feng, Zhi Dong, Shuyu Zhuo, Bihui Zhong

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引用次数: 0

Abstract

Cross-sectional studies have demonstrated the association of skeletal muscle mass with metabolic-associated fatty liver disease (MAFLD), while longitudinal data are scarce. We aimed to explore the impact of changes in relative skeletal muscle mass on the MAFLD treatment response. MAFLD patients undergoing magnetic resonance imaging-based proton density fat fraction for liver fat content (LFC) assessments and bioelectrical impedance analysis before and after treatment (orlistat, meal replacement, lifestyle modifications) were enrolled. Appendicular muscle mass (ASM) was adjusted by weight (ASM/W). Overall, 256 participants were recruited and divided into two groups: with an ASM/W increase (n=166) and without an ASM/W increase (n=90). There was a great reduction in LFC in the group with an ASM/W increase (16.9% versus 8.2%, P < 0.001). However, the change in LFC in the group without an ASM/W increase showed no significant difference (12.5% versus 15.0%, P > 0.05). △ASM/W Follow-up-Baseline [odds ratio (OR)=1.48, 95% confidence interval (CI) 1.05-2.07, P = 0.024] and △total fat mass (OR=1.45, 95% CI 1.12-1.87, P = 0.004) were independent predictors for steatosis improvement (relative reduction of LFC ≥ 30%). The subgroup analysis showed that, despite without weight loss, decrease in HOMA-IR (OR=6.21, 95% CI 1.28-30.13, P=0.023), △total fat mass Baseline -Follow-up (OR=3.48, 95% CI 1.95-6.21, P <0.001 and △ASM/W Follow-up-Baseline (OR=2.13, 95% CI 1.12-4.05, P=0.022) independently predicted steatosis improvement. ASM/W increase and loss of total fat mass benefit the resolution of liver steatosis, independent of weight loss for MAFLD.

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恢复骨骼肌质量是改善 MAFLD 患者肝脏脂肪沉积的独立决定因素

横断面研究表明，骨骼肌质量与代谢相关性脂肪肝（MAFLD）有关，但纵向数据却很少。我们旨在探索骨骼肌相对质量的变化对 MAFLD 治疗反应的影响。我们招募了在治疗（奥利司他、代餐、生活方式调整）前后接受基于磁共振成像的质子密度脂肪分数肝脏脂肪含量（LFC）评估和生物电阻抗分析的 MAFLD 患者。腓肠肌质量（ASM）根据体重（ASM/W）进行调整。总共招募了 256 名参与者，分为两组：ASM/W 增加组（166 人）和 ASM/W 未增加组（90 人）。ASM/W 增加组的 LFC 显著降低（16.9% 对 8.2%，P < 0.001）。然而，未提高 ASM/W 组的 LFC 变化无显著差异（12.5% 对 15.0%，P > 0.05）。△ASM/W随访-基线[几率比（OR）=1.48，95% 置信区间（CI）1.05-2.07，P = 0.024]和△总脂肪量（OR=1.45，95% CI 1.12-1.87，P = 0.004）是脂肪变性改善（LFC相对减少≥30%）的独立预测因素。亚组分析表明，尽管体重没有减轻，HOMA-IR的下降（OR=6.21，95% CI 1.28-30.13，P=0.023）、△总脂肪量基线-随访（OR=3.48，95% CI 1.95-6.21，P<0.001）和△ASM/W随访-基线（OR=2.13，95% CI 1.12-4.05，P=0.022）独立预测了脂肪变性的改善。ASM/W的增加和总脂肪量的减少有利于肝脏脂肪变性的缓解，与MAFLD的体重减轻无关。

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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来源期刊

Skeletal Muscle CELL BIOLOGY-

CiteScore

9.10

自引率

0.00%

发文量

审稿时长

12 weeks

期刊介绍： The only open access journal in its field, Skeletal Muscle publishes novel, cutting-edge research and technological advancements that investigate the molecular mechanisms underlying the biology of skeletal muscle. Reflecting the breadth of research in this area, the journal welcomes manuscripts about the development, metabolism, the regulation of mass and function, aging, degeneration, dystrophy and regeneration of skeletal muscle, with an emphasis on understanding adult skeletal muscle, its maintenance, and its interactions with non-muscle cell types and regulatory modulators. Main areas of interest include: -differentiation of skeletal muscle- atrophy and hypertrophy of skeletal muscle- aging of skeletal muscle- regeneration and degeneration of skeletal muscle- biology of satellite and satellite-like cells- dystrophic degeneration of skeletal muscle- energy and glucose homeostasis in skeletal muscle- non-dystrophic genetic diseases of skeletal muscle, such as Spinal Muscular Atrophy and myopathies- maintenance of neuromuscular junctions- roles of ryanodine receptors and calcium signaling in skeletal muscle- roles of nuclear receptors in skeletal muscle- roles of GPCRs and GPCR signaling in skeletal muscle- other relevant aspects of skeletal muscle biology. In addition, articles on translational clinical studies that address molecular and cellular mechanisms of skeletal muscle will be published. Case reports are also encouraged for submission. Skeletal Muscle reflects the breadth of research on skeletal muscle and bridges gaps between diverse areas of science for example cardiac cell biology and neurobiology, which share common features with respect to cell differentiation, excitatory membranes, cell-cell communication, and maintenance. Suitable articles are model and mechanism-driven, and apply statistical principles where appropriate; purely descriptive studies are of lesser interest.