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体重反弹而非减轻会加剧雄性小鼠多次体重循环事件中的肝纤维化。

Weight regain, but not weight loss exacerbates hepatic fibrosis during multiple weight cycling events in male mice.

机构信息

Department of Animal Science and Technology, National Taiwan University, Taipei, Taiwan.

Institute of Biotechnology, National Taiwan University, Taipei, Taiwan.

出版信息

Eur J Nutr. 2024 Apr;63(3):965-976. doi: 10.1007/s00394-024-03326-w. Epub 2024 Jan 24.

DOI:10.1007/s00394-024-03326-w
PMID:38265751
Abstract

PURPOSE

Weight cycling is a phenomenon characterized by fluctuating body weight that is commonly observed in individuals employing intentional weight loss methods. Despite its prevalence, the impact of weight cycling on health remains equivocal. The current investigation aimed to examine the effects of weight cycling on liver health.

METHODS

The weight cycling model was established by switching the feeding method of mice between ad libitum (AL) and restricted intake (DR or 60% of AL) of the breeding diet to cause weight gain and weight loss, respectively. The weight cycling model comprised two and a half cycles, with one group terminating the experience during the weight-gain period (S-AL) and the other during the weight-loss period (S-DR). Liver tissue was collected to investigate morphology alterations, apoptosis, lipid metabolism, and mitochondrial homeostasis.

RESULTS

The results demonstrated that the termination point of weight cycling affected body weight and hepatic steatosis. All parameters examined in the S-DR mice exhibited a comparable trend to those observed in the DR mice. Notably, S-AL mice showed a significant increase in lipid metabolism-related proteins in the liver compared to AL-fed mice, along with reduced lipid droplets. Moreover, hepatic apoptosis and fibrosis were exacerbated in the S-AL mice compared to AL mice, whereas mitochondrial fusion, biogenesis, and mitophagy were decreased in the S-AL mice.

CONCLUSION

Weight cycling ending in weight gain exacerbated hepatic fibrosis, potentially by inducing apoptosis or disrupting mitochondrial homeostasis. Conversely, weight cycling ending in weight loss demonstrated beneficial effects on hepatic health.

摘要

目的

体重波动是一种体重波动的现象,在采用有意减肥方法的个体中较为常见。尽管体重波动很常见,但它对健康的影响仍存在争议。本研究旨在探讨体重波动对肝脏健康的影响。

方法

通过在自由进食(AL)和限制摄入(DR 或 AL 的 60%)繁殖饮食之间切换来建立体重波动模型,分别导致体重增加和体重减轻。体重波动模型包括两个半周期,一组在体重增加期结束(S-AL),另一组在体重减轻期结束(S-DR)。收集肝组织以研究形态改变、细胞凋亡、脂质代谢和线粒体稳态。

结果

结果表明,体重波动的终止点会影响体重和肝脂肪变性。S-DR 小鼠的所有检查参数均表现出与 DR 小鼠相似的趋势。值得注意的是,与 AL 喂养的小鼠相比,S-AL 小鼠的肝脏中与脂质代谢相关的蛋白显著增加,并且脂质滴减少。此外,与 AL 小鼠相比,S-AL 小鼠的肝凋亡和纤维化加剧,而 S-AL 小鼠的线粒体融合、生物发生和自噬减少。

结论

以体重增加结束的体重波动加重了肝纤维化,可能通过诱导细胞凋亡或破坏线粒体稳态。相反,以体重减轻结束的体重波动对肝脏健康有益。

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线粒体稳态:生物学及其在肝脂肪变性向 NASH 的作用。
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