Major in Sport Science, Division of Sport Industry and Science, College of Performing Arts and Sport, Hanyang University, 222 Wangsimni-ro, Seongdong-gu, Seoul, Republic of Korea.
BK21 FOUR Human-Tech Convergence Program, Hanyang University, 222 Wangsimni-ro, Seongdong-gu, Seoul 04763, Republic of Korea.
Biosci Rep. 2024 Nov 27;44(11). doi: 10.1042/BSR20240784.
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.
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.
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.
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.
单纯衰弱和肥胖衰弱是衰弱综合征的常见类型。然而，单纯衰弱和肥胖衰弱之间的重叠和独特特征尚不清楚。本研究旨在揭示单纯衰弱和肥胖衰弱的重叠/独特的身体和生物学表型，为其预防、诊断和治疗提供理论依据。
用正常或高脂肪饮食喂养小鼠，并在 20 个月大时进行评估。将它们分为对照组、肥胖组、单纯衰弱组和肥胖衰弱组。通过测量握力、行走速度、身体活动、耐力和体重来确定单纯衰弱和肥胖衰弱。评估身体和生物学表型。
在体重、瘦体重、脂肪量、组织脂肪量、握力、耐力和身体活动方面，单纯衰弱和肥胖衰弱之间存在明显的身体表型差异，而行走速度则重叠。在生物学表型方面，Smad2/3、FoxO3a、P62、LAMP-2 和组织蛋白酶 L 的表达水平存在明显差异，而 AKT、p-AKT、mTOR、p-mTOR、p-Smad2/3、p-FoxO3a、Beclin-1、ATG7 和 LC3 则重叠。
肥胖衰弱中观察到的明显的身体表型主要归因于肥胖的影响，衰弱综合征和肥胖的联合作用进一步损害了肌肉功能。单纯衰弱和肥胖衰弱具有重叠的生物学表型，特别是在肌肉蛋白合成的调节方面。此外，肥胖和衰弱综合征之间的相互作用产生了重叠和独特的生物学表型，特别是在特定降解信号蛋白的调节方面。
