Ameka Magdalene K, Hasty Alyssa H
Department of Molecular Physiology and Biophysics, Vanderbilt University, 23rd Ave South and Pierce, Nashville 37232-0615 USA.
Immunometabolism. 2020;2(4). doi: 10.20900/immunometab20200034. Epub 2020 Oct 8.
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.
低度慢性脂肪组织（AT）炎症现已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；脂肪组织巨噬细胞（ATM）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铁稳态的核心调节因子。在最佳条件下，ATM维持脂肪细胞中铁的适当稳态平衡；然而，在肥胖期间，这种关系会发生改变，铁会重新分配到脂肪细胞中，而不是ATM中。这种脂肪细胞铁过载会导致全身性胰岛素抵抗（IR），这些影响的机制仍在研究中。在此，我们对最近关于脂肪细胞和ATM铁处理之间相互作用以及代谢功能障碍的研究结果进行评论。
