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中年运动对衰老小鼠脂质代谢的影响:与终身运动相当,优于中年停止运动。

Effect of midlife exercise on lipid metabolism in aging mice: comparable to lifelong exercise, better than ceasing midlife exercise.

作者信息

Yang Ling, Peng Tuanhui, Yan Xu, Lin Pengjie

机构信息

School of Physical Education, Shaoguan University, Shaoguan, 512000, Guangdong, China.

Institute for Health and Sport, Victoria University, Melbourne, VIC, 8001, Australia.

出版信息

Sci Rep. 2025 Apr 11;15(1):12531. doi: 10.1038/s41598-025-97140-x.

DOI:10.1038/s41598-025-97140-x
PMID:40216894
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11992076/
Abstract

This study examines the effects of continuous versus interrupted lifelong exercise on lipid metabolism in naturally aging male BALB/c mice. Five-week-old male BALB/c mice were randomly assigned to five groups: young control group (YC), natural ageing control group (AC), exercise cessation group (DE), middle-aged commencing exercise group (ME), and lifelong exercise group (LE). Moderate Intensity Continuous Training exercise sessions were conducted three times per week, with each session lasting 50 min; after exercise interventions until 72 weeks of age, the following parameters were measured: body morphology, exercise capacity, blood lipid, liver fat content, liver function, expression of liver lipid metabolism-related genes and endoplasmic reticulum stress-related genes, and activities of liver metabolism enzymes. The results suggest that advancing age leads to disrupted lipid processing, reduced hepatic performance, and increased endoplasmic reticular tension. Compared with the AC group, the ME and LE cohorts showed reduced serum lipids, whereas the LE group exhibited elevated high-density lipoprotein cholesterol (HDL-C) levels (P < 0.05). Post-exercise reductions were observed in hepatic total cholesterol and free fatty acid (FFA). Moreover, the exercises mitigated age-related hepatic impairments and diminished susceptibility towards cirrhosis despite higher aspartate aminotransferase (AST) and lower albumin (ALB) levels being evident within the DE cohort (P < 0.05). Exercise demonstrates the potential to mitigate age-related abnormalities in lipid metabolism. Middle-aged commencing and lifelong exercise interventions are more effective in alleviating lipid abnormalities than exercise cessation in middle age. This disparity in efficacy can be attributed to differences in regulating endoplasmic reticulum stress, enhancing liver lipid oxidation capacity, and reducing lipid synthesis ability. Notably, middle-aged individuals commencing exercise yield similar outcomes in regulating aging-associated abnormal lipid metabolism compared to the lifelong exercise group. This highlights the importance of initiating exercise in middle age, as it remains beneficial even if lifelong commitment is unfeasible, so exercise initiation in midlife is still beneficial. However, to prevent liver lipid metabolism disorders later in life, the earlier exercise initiation, the better.

摘要

本研究考察了持续终身运动与间断终身运动对自然衰老雄性BALB/c小鼠脂质代谢的影响。将5周龄雄性BALB/c小鼠随机分为五组:青年对照组(YC)、自然衰老对照组(AC)、运动停止组(DE)、中年开始运动组(ME)和终身运动组(LE)。采用中等强度持续训练,每周进行3次,每次持续50分钟;运动干预至72周龄后,测量以下参数:身体形态、运动能力、血脂、肝脏脂肪含量、肝功能、肝脏脂质代谢相关基因和内质网应激相关基因的表达以及肝脏代谢酶活性。结果表明,年龄增长导致脂质加工紊乱、肝脏功能下降和内质网张力增加。与AC组相比,ME组和LE组血清脂质降低,而LE组高密度脂蛋白胆固醇(HDL-C)水平升高(P<0.05)。运动后肝脏总胆固醇和游离脂肪酸(FFA)降低。此外,尽管DE组天冬氨酸转氨酶(AST)水平较高、白蛋白(ALB)水平较低(P<0.05),但运动减轻了与年龄相关的肝脏损伤,降低了肝硬化易感性。运动显示出减轻与年龄相关的脂质代谢异常的潜力。中年开始运动和终身运动干预在缓解脂质异常方面比中年停止运动更有效。这种疗效差异可归因于内质网应激调节、肝脏脂质氧化能力增强和脂质合成能力降低的差异。值得注意的是,中年开始运动的个体在调节与衰老相关的异常脂质代谢方面与终身运动组产生相似的结果。这突出了中年开始运动的重要性,因为即使无法终身坚持运动,中年开始运动仍然有益,所以中年开始运动仍然是有益的。然而,为了预防晚年肝脏脂质代谢紊乱,运动开始得越早越好。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/feaf/11992076/d0134aaac376/41598_2025_97140_Fig9_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/feaf/11992076/4b8e48418aa8/41598_2025_97140_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/feaf/11992076/dce7e96be14a/41598_2025_97140_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/feaf/11992076/97d35af9c678/41598_2025_97140_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/feaf/11992076/d0134aaac376/41598_2025_97140_Fig9_HTML.jpg

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