转录组学分析表明,肌肉质量的调节因子在与年龄相关的肌肉减少性肥胖中发生了改变。

IF 3.7 2区 生物学 Q2 BIOTECHNOLOGY & APPLIED MICROBIOLOGY
Eleanor R Schrems, Ana Regina Cabrera, Ronald G Jones, Francielly Morena, Kevin A Murach, Nicholas P Greene, Tyrone A Washington
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引用次数: 0

摘要

背景:肌少性肥胖(Sarcopenic obesity, SO)是一种肌少症和肥胖的合并病症,常见于老年人群。SO与身体功能差、肌肉骨骼损伤风险增加、生活质量和独立性降低有关。关于这种情况的分子基础的信息是有限的。本研究的目的是提供一种转录组学分析,表征终身肥胖诱导的SO,并提供对该病病因的更深入了解。结果:幼龄(Y)(6个月)和老龄(A)(21-24个月)小鼠可随意饲喂正常饲料(L)(12%卡路里来自脂肪)或高脂肪饲料(O)(60%卡路里来自脂肪)。通过多项分析,我们观察到与YO相比,AO中与ECM重塑相关的基因下调,从而深入了解年龄对终身肥胖状况的影响。此外,我们观察到与慢肌纤维收缩和快到慢肌纤维类型转换相关的基因在老年状态下随着肥胖而上调。综上所述,我们的研究结果揭示了SO骨骼肌失调的特定途径,提供了分子见解,增强了我们对这种情况下导致肌肉功能受损的潜在机制的理解。进一步探索这些失调对于确定针对SO中肌肉功能损伤来源的治疗方法至关重要。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Transcriptomic analysis demonstrates moderators of muscle quality are altered in age-related sarcopenic obesity.

Background: Sarcopenic obesity (SO) is the combined condition of sarcopenia and obesity, which commonly occurs in the older adult population. SO is associated with poor physical function, increased risk of musculoskeletal injury, and reduced quality of life and independence. Information on the molecular underpinnings of this condition is limited. The aim of this study was to provide a transcriptomic analysis characterizing SO induced by lifelong obesity and to provide a deeper understanding of the etiology of the condition.

Results: Young (Y) (6 mo) and aged (A) (21-24 mo) mice were fed either normal chow (L) (12% kcal from fat) or high-fat (O) (60% kcal from fat) diets ad libitum. Through multiple analyses, we observed that genes related to ECM remodeling were downregulated in AO compared with YO, providing insight into the effects of age in a life-long obese condition. Furthermore, we observed that genes related to contraction in slow-twitch muscle fibers and fast-to-slow muscle fiber type transitions were upregulated with obesity in the aged condition.

Conclusion: Taken together, our findings reveal specific pathways of dysregulation in SO skeletal muscle, offering molecular insights that enhance our understanding of the underlying mechanisms contributing to impaired muscle function in this condition. Further exploration of these dysregulations is critical to identifying therapeutic treatments targeting the source of muscle functional impairment in SO.

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来源期刊
BMC Genomics
BMC Genomics 生物-生物工程与应用微生物
CiteScore
7.40
自引率
4.50%
发文量
769
审稿时长
6.4 months
期刊介绍: BMC Genomics is an open access, peer-reviewed journal that considers articles on all aspects of genome-scale analysis, functional genomics, and proteomics. BMC Genomics is part of the BMC series which publishes subject-specific journals focused on the needs of individual research communities across all areas of biology and medicine. We offer an efficient, fair and friendly peer review service, and are committed to publishing all sound science, provided that there is some advance in knowledge presented by the work.
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