Overlapping and Distinct Physical and Biological Phenotypes in Pure Frailty and Obese Frailty.

IF 3.8 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Bioscience Reports Pub Date : 2024-11-27 DOI:10.1042/BSR20240784
Fujue Ji, Ji Hyun Park, Hyeonseung Rheem, Jong-Hee Kim
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Abstract

Background: Pure frailty and obese frailty are common types of frailty syndrome. However, the overlapping and distinct characteristics between pure frailty and obese frailty remain unclear. This study aims to reveal the overlapping/distinct physical and biological phenotypes of pure frailty and obese frailty, providing theoretical support for their prevention, diagnosis, and treatment.

Method: Mice were fed either a normal or high-fat diet and assessed at 20 months of age. They were assigned to one of the four groups: control, obesity, pure frailty, and obese frailty. Grip strength, walking speed, physical activity, endurance, and body weight were measured to determine pure frailty and obese frailty. Physical and biological phenotypes were assessed.

Results: Distinct physical phenotypes were observed between pure frailty and obese frailty in terms of body weight, lean mass, fat mass, fat mass in tissue, grip strength, endurance, and physical activity, while walking speed overlapped. In biological phenotypes, levels of Smad2/3, FoxO3a, P62, LAMP-2, and cathepsin L expression were distinct, while AKT, p-AKT, mTOR, p-mTOR, p-Smad2/3, p-FoxO3a, Beclin-1, ATG7, and LC3 overlapped.

Conclusion: Distinct physical phenotypes observed in obese frailty are primarily attributable to the effect of obesity, with further impairment of muscle function resulting from the combined effects of frailty syndromes and obesity. Pure frailty and obese frailty share overlapping biological phenotypes, particularly in the regulation of muscle protein synthesis. Moreover, the interaction between obesity and frailty syndromes gives rise to both overlapping and distinct biological phenotypes, especially in the regulation of specific degradation signaling proteins.

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与纯粹虚弱和虚弱肥胖相关的重叠和不同的生理和生物表型。
背景: 单纯性虚弱和肥胖性虚弱是虚弱综合征的常见类型。然而,单纯性虚弱和肥胖性虚弱之间的重叠和不同特征仍不清楚。本研究旨在揭示单纯性虚弱和肥胖性虚弱在生理和生物学表型上的重叠/区别,为其预防、诊断和治疗提供理论支持:用正常或高脂肪饮食喂养小鼠,在小鼠 20 个月大时对其进行评估。它们被分配到四组中的一组:对照组、肥胖组、纯虚弱组和肥胖虚弱组。通过测量握力、行走速度、体力活动、耐力和体重来确定纯虚弱组和肥胖虚弱组。对身体和生物表型进行了评估:在体重、瘦体重、脂肪量、组织中的脂肪量、握力、耐力和体力活动方面,纯粹虚弱和肥胖虚弱之间观察到了不同的物理表型,而步行速度则有重叠。在生物表型方面,Smad2/3、FoxO3a、P62、LAMP-2 和 cathepsin L 的表达水平不同,而 AKT、p-AKT、mTOR、p-mTOR、p-Smad2/3、p-FoxO3a、Beclin-1、ATG7 和 LC3 的表达水平重叠:在肥胖性虚弱中观察到的不同身体表型主要归因于肥胖的影响,而虚弱综合征和肥胖的共同影响会进一步损害肌肉功能。单纯性虚弱和肥胖性虚弱在生物学表型上有重叠之处,尤其是在肌肉蛋白质合成的调节方面。此外,肥胖和虚弱综合征之间的相互作用会产生既重叠又不同的生物表型,特别是在调节特定降解信号蛋白方面。
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来源期刊
Bioscience Reports
Bioscience Reports 生物-细胞生物学
CiteScore
8.50
自引率
0.00%
发文量
380
审稿时长
6-12 weeks
期刊介绍: Bioscience Reports provides a home for sound scientific research in all areas of cell biology and molecular life sciences. Since 2012, Bioscience Reports has been fully Open Access and publishes all papers under the liberal CC BY licence, giving the life science community quality research to share and discuss.Content before 2012 is subscription-only, and is accessible via archive purchase. Articles are assessed on soundness, providing a home for valid findings and data. We welcome papers that span disciplines (e.g. chemistry, medicine), including papers describing: -new methodologies -tools and reagents to probe biological questions -mechanistic details -disease mechanisms -metabolic processes and their regulation -structure and function -bioenergetics
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