Cell Reports：部分人群过多摄入铁元素会增加患肠癌风险

现在有许多补铁的广告，但英国一项最新研究显示，部分人群不宜过多摄入铁元素，因为这会增加他们患肠癌的风险。

英国伯明翰大学等机构的研究人员在新一期《细胞—报告》杂志上发表论文说，动物实验显示，在同样摄入较多铁元素的情况下，基因APC有缺陷的实验鼠与没有缺陷的实验鼠相比，出现肠癌的风险是后者的两三倍。而基因APC有缺陷的实验鼠如果要避免肠癌，则需要使其饮食中的铁元素含量非常少。

据介绍，人类肠癌患者中也有类似情况，约十分之八的肠癌患者都属于基因APC有缺陷的人群。因此，基因APC有缺陷的人群不适宜过多摄入铁元素。

参与研究的克里斯·采莱皮什说，这项研究证实了基因缺陷与摄入过多铁元素会共同导致肠癌风险升高，研究人员正在这个发现的基础上探索相应治疗方法，即想办法降低肠道内铁元素的含量，从而降低肠癌风险，并希望能在接下来几年内开展人类临床试验。

铁元素在猪肉、牛肉等“红肉”中含量较高，并且过去也有医学研究显示常吃红肉的人群肠癌风险较高。英国卫生部曾为此专门发布饮食建议，希望那些每天食用超过90克红肉的人，应该将摄入量降到英国的平均水平70克。这一水平在英国的食谱中，相当于两个标准大小的牛肉汉堡以及一块羊排或三片火腿肉。

DOI:10.1016/j.celrep.2012.07.003
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Luminal Iron Levels Govern Intestinal Tumorigenesis after Apc Loss In Vivo

Sorina Radulescu, Matthew J. Brookes, Pedro Salgueiro, Rachel A. Ridgway, Ewan McGhee, Kurt Anderson, Samuel J. Ford, Daniel H. Stones, Tariq H. Iqbal, Chris Tselepis, Owen J. Sansom

It is clear from epidemiological studies that excess iron is associated with increased risk of colorectal cancer; however, questions regarding the mechanism of how iron increases cancer risk, the source of the excess iron (circulating or luminal), and whether iron reduction represents a potential therapeutic option remain unanswered. In this study, we show that after Apc deletion, the cellular iron acquisition proteins TfR1 and DMT1 are rapidly induced. Conversely, restoration of APC reduces cellular iron due to repression of these proteins. To test the functional importance of these findings, we performed in vivo investigations of the impact of iron levels on intestinal tumorigenesis. Strikingly, depletion of luminal (but not systemic) iron strongly suppressed murine intestinal tumorigenesis, whereas increased luminal iron strongly promoted tumorigenesis. Taken together, our data definitively delineate iron as a potent modifier of intestinal tumorigenesis and have important implications for dietary iron supplementation in patients at high risk of colorectal cancer.