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肥胖会通过AFABP介导的肠干细胞的铁过载损害肠道修复

Zhiming Liu¹, Yi Chen², Jinhua Yan¹

¹West China Centre of Excellence for Pancreatitis, and Laboratory of Metabolism and Aging, Frontiers Science Center for Disease-related Molecular Network, National Clinical Research Center for Geriatrics, West China Hospital, Sichuan University, Chengdu, China.

Nature metabolism

|January 8, 2026

概括

肥胖会通过增加脂肪细胞脂肪酸结合蛋白 (AFABP) 来阻碍肠道修复,这会破坏肠道干细胞 (ISC) 中的铁平衡. 准这种脂肪肠轴可以治疗与肥胖相关的肠道问题.

科学领域:

胃肠病学胃肠病学
代谢障碍代谢障碍代谢障碍
细胞生物学细胞生物学

背景情况:

肥胖会对器官功能产生负面影响,但其对肠道再生的具体影响尚未完全理解.
肠干细胞 (ISC) 对于受伤后的肠道修复至关重要.
脂肪细胞脂肪酸结合蛋白 (AFABP) 在脂肪酸运输中发挥作用,并与代谢疾病有关.

研究的目的:

调查AFABP在肥胖损害肠道修复中的作用.
阐明AFABP影响肠道干细胞和肠道再生的分子机制.
为了确定与肥胖相关的肠道疾病的潜在治疗点.

主要方法:

在肥胖和瘦小鼠模型中研究了AFABP对肠干细胞 (ISC) 铁稳态的影响.
研究了AFABP对过氧体介导的ISC差异化的影响.
评估了AFABP抑制剂,铁化剂和过氧体激活剂在减轻肥胖小鼠大肠炎中的治疗潜力.

主要成果:

肥胖症中AFABP升高会通过与转激素结合来破坏ISC中的铁稳态,从而导致铁的积累.
在ISC中积累的铁会损害过氧体介导的分化,阻碍肠道的修复.
在肥胖动物中,AFABP的枯竭,抑制,铁化或过氧体激活改善了大肠炎.

结论:

AFABP是一个关键的调解者,通过破坏ISC铁的稳态和分化,将肥胖与肠道修复功能受损联系起来.
脂肪肠轴是治疗肥胖相关肠道并发症的有希望的治疗点.
调节AFABP活动或铁水平为治疗与肥胖相关的肠道疾病提供了潜在的策略.

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