Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI, United States; Department of Cellular and Molecular Biology, University of Michigan, Ann Arbor, MI, United States; Medical Scientist Training Program, University of Michigan, Ann Arbor, MI, United States.
Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI, United States.
J Nutr. 2024 Apr;154(4):1153-1164. doi: 10.1016/j.tjnut.2024.01.013. Epub 2024 Jan 19.
Tissue repair and regeneration in the gastrointestinal system are crucial for maintaining homeostasis, with the process relying on intricate cellular interactions and affected by micro- and macro-nutrients. Iron, essential for various biological functions, plays a dual role in tissue healing by potentially causing oxidative damage and participating in anti-inflammatory mechanisms, underscoring its complex relationship with inflammation and tissue repair.
The study aimed to elucidate the role of low dietary iron in gastrointestinal tissue repair.
We utilized quantitative iron measurements to assess iron levels in inflamed regions of patients with ulcerative colitis and Crohn's disease. In addition, 3 mouse models of gastrointestinal injury/repair (dextran sulfate sodium-induced colitis, radiation injury, and wound biopsy) were used to assess the effects of low dietary iron on tissue repair.
We found that levels of iron in inflamed regions of both patients with ulcerative colitis and Crohn's disease are elevated. Similarly, during gastrointestinal repair, iron levels were found to be heightened, specifically in intestinal epithelial cells across the 3 injury/repair models. Mice on a low-iron diet showed compromised tissue repair with reduced proliferation. In standard diet, epithelial cells and the stem cell compartment maintain adequate iron stores. However, during a period of iron deficiency, epithelial cells exhaust their iron reserves, whereas the stem cell compartments maintain their iron pools. During injury, when the stem compartment is disrupted, low iron levels impair proliferation and compromise repair mechanisms.
Low dietary iron impairs intestinal repair through compromising the ability of epithelial cells to aid in intestinal proliferation.
胃肠道组织的修复和再生对于维持内环境稳定至关重要，这一过程依赖于复杂的细胞相互作用，并受到微营养素和宏营养素的影响。铁是多种生物功能所必需的，它在组织愈合中具有双重作用，一方面可能导致氧化损伤，另一方面参与抗炎机制，这突出了其与炎症和组织修复的复杂关系。
本研究旨在阐明低膳食铁在胃肠道组织修复中的作用。
我们利用定量铁测量来评估溃疡性结肠炎和克罗恩病患者炎症区域的铁水平。此外，还使用了 3 种胃肠道损伤/修复的小鼠模型（葡聚糖硫酸钠诱导的结肠炎、辐射损伤和伤口活检）来评估低膳食铁对组织修复的影响。
我们发现溃疡性结肠炎和克罗恩病患者炎症区域的铁水平升高。同样，在胃肠道修复过程中，我们发现铁水平升高，特别是在 3 种损伤/修复模型中的肠上皮细胞中。低铁饮食的小鼠表现出组织修复受损，增殖减少。在标准饮食中，上皮细胞和干细胞区室维持足够的铁储存。然而，在缺铁期间，上皮细胞耗尽了铁储备，而干细胞区室则维持其铁池。在损伤期间，当干细胞区室受到干扰时，低铁水平会损害增殖并损害修复机制。
低膳食铁通过削弱上皮细胞促进肠道增殖的能力来损害肠道修复。
