Blachier François, Vaugelade Pierre, Robert Véronique, Kibangou Bertille, Canonne-Hergaux François, Delpal Serge, Bureau François, Blottière Hervé, Bouglé Dominique
Laboratoire de Nutrition et Sécurité Alimentaire, Institut National de la Recherche Agronomique, 78350 Jouy-en-Josas, France.
Can J Physiol Pharmacol. 2007 Feb;85(2):185-92. doi: 10.1139/y07-007.
Iron deficiency is the most common human nutritional disorder in the world. Iron absorptive capacity of the small intestine is known to be much limited and therefore large quantities of iron salts must be used to treat iron deficiency. As a result, significant amounts of iron may reach the large intestine. This study compared the capacities of the small and large intestine to transfer luminal iron to the venous blood in relationship with the expression in epithelial cells of proteins involved in iron absorption using a pig model. Intracaecal injection of iron sulphate corresponding with 2.5 and 5.0 mg elemental iron per kg body mass resulted in modest, transient, but significant (p<0.05) increases in iron concentration in the portal blood plasma. By comparing portal blood plasma iron concentrations following injection in the duodenal and caecal lumen, we calculated that 5 h after injection, iron colonic absorption represented approximately 14% of duodenal absorption. Caecal and proximal colon mucosa accumulated iron to a much lower extent than the duodenal mucosa. Isolated colonocytes were found to express divalent metal transporter (DMT1) and ferritin, but to a lesser extent than the duodenal enterocytes. Ferroportin was highly expressed in colonocytes. In these cells as well as in enterocytes ferroportin was found to be glycosylated. In short term experiments and at a concentration in the range of that measured in the aqueous phases recovered from the large intestine luminal content after iron injection, iron sulphate did not alter colonocyte viability. We concluded that the colonic epithelial cells that express proteins involved in iron absorption are able to transfer luminal iron to the venous blood even if its relative participation in the overall intestinal absorption appears to be modest under our experimental conditions.
缺铁是全球最常见的人类营养紊乱症。已知小肠的铁吸收能力非常有限，因此必须使用大量铁盐来治疗缺铁。结果，大量的铁可能会进入大肠。本研究使用猪模型，比较了小肠和大肠将肠腔铁转运至静脉血的能力，并研究了其与铁吸收相关蛋白在上皮细胞中的表达情况。向盲肠内注射每千克体重对应2.5毫克和5.0毫克元素铁的硫酸铁，导致门静脉血浆中铁浓度适度、短暂但显著（p<0.05）升高。通过比较十二指肠和盲肠腔注射后门静脉血浆中铁浓度，我们计算出注射后5小时，结肠对铁的吸收约占十二指肠吸收的14%。盲肠和近端结肠黏膜中铁的积累程度远低于十二指肠黏膜。分离的结肠细胞被发现表达二价金属转运体（DMT1）和铁蛋白，但表达程度低于十二指肠肠上皮细胞。铁转运蛋白在结肠细胞中高度表达。在这些细胞以及肠上皮细胞中，铁转运蛋白被发现发生了糖基化。在短期实验中，在铁注射后从大肠腔内容物中回收的水相中测得的浓度范围内，硫酸铁不会改变结肠细胞的活力。我们得出结论，即使在我们的实验条件下，结肠上皮细胞中表达的参与铁吸收的蛋白将肠腔铁转运至静脉血的相对比例似乎较小，但它们仍能够完成这一过程。
