脂肪和铁不能混合。

Immunometabolism Pub Date : 2020-01-01 Epub Date: 2020-10-08 DOI:10.20900/immunometab20200034
Magdalene K Ameka, Alyssa H Hasty
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引用次数: 5

摘要

低级别慢性脂肪组织(AT)炎症现在被认为是与肥胖相关并发症相关的多器官功能障碍的关键驱动因素;和脂肪组织巨噬细胞(ATMs)是这种炎症环境发展的关键。除了在免疫监视中的作用外,atm还是AT铁稳态的主要调节者。在最佳条件下,atm在脂肪细胞中维持适当的铁稳态平衡;然而,在肥胖期间,这种关系被改变,铁被重新分配到脂肪细胞中,而不是atm。脂肪细胞铁超载导致系统性IR,这些影响的机制仍在研究中。在此,我们对脂肪细胞和ATM铁处理之间的相互作用以及代谢功能障碍的最新发现进行了评论。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Fat and Iron Don't Mix.

Low-grade chronic adipose tissue (AT) inflammation is now recognized as a pivotal driver of the multi-organ dysfunction associated with obesity-related complications; and adipose tissue macrophages (ATMs) are key to the development of this inflammatory milieu. Along with their role in immunosurveillance, ATMs are central regulators of AT iron homeostasis. Under optimal conditions, ATMs maintain a proper homeostatic balance of iron in adipocytes; however, during obesity, this relationship is altered, and iron is repartitioned into adipocytes as opposed to ATMs. This adipocyte iron overload leads to systemic IR and the mechanism for these effects is still under investigation. Here, we comment on the most recent findings addressing the interplay between adipocyte and ATM iron handling, and metabolic dysfunction.

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