|Tako, Elad - CORNELL UNIVERSITY|
|Lei, Xingen - CORNELL UNIVERSITY|
|Yasuda, K - CORNELL UNIVERSITY|
|Miller, Dennis - CORNELL UNIVERSITY|
Submitted to: British Journal of Nutrition
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: July 1, 2007
Publication Date: March 1, 2008
Citation: Tako, E., Glahn, R.P., Welch, R.M., Lei, X., Yasuda, K., Miller, D. 2008. Dietary inulin affects the expression of intestinal enterocyte iron transporters, receptors and storage protein and alters the microbiota in the pig intestine. British Journal of Nutrition. 99:472-480. Interpretive Summary: Iron deficiency afflicts over half of the world’s population primarily from low available iron levels in diets dominated by staple plant foods that contain antinutrients that inhibit iron absorption from the gut. Certain substances can promote iron absorption from diets high in antinutrients such as phytate. Inulin, a non-digestible fructan carbohydrate is such a promoter substance. Just how inulin promotes iron absorption from the gut is not known. We studied the effects of inulin on the expression of iron transporter and receptor protein genes in pig intestinal enterocytes. Inulin induced the expression of a number of genes responsible for the absorption of iron from the gut. It also stimulated the growth of beneficial bacteria in the pig intestine. The results of this research suggest that inulin may trigger the up-regulation of genes encoding iron uptake from the gut but the specific mechanisms of the stimulation remain to be elucidated.
Technical Abstract: Inulin, a linear beta fructan, is present in a variety of plants including chicory root and wheat. It exhibits prebiotic properties and was shown to enhance mineral absorption and increase beneficial bacteria in the colon. The aim of this study was to assess the effect of dietary inulin on selected intestinal iron transporters and binding proteins gene expression. Anemic piglets at age 5 weeks were allocated to a standard corn-soy diet (control) or the same diet supplemented with inulin at a level of 4%. After 6 weeks, the animals were killed and cecum contents and sections of the duodenum and colon were removed. Segments of the genes encoding for the pig divalent metal transporter 1 (DMT1) and duodenal cytochrome-b reductase (Dcytb) were isolated and sequenced. Semi quantitative RT-PCR analyses were performed to evaluate the expression of DMT1, Dcytb, ferroportin, ferritin, transferrin receptor (TfR), mucin genes. DMT1, Dcytb, ferroportin, ferritin, and TfR mRNA levels in duodenal samples were significantly higher in the inulin group (P = 0.05) compared to the control. In colon, DMT1, TfR and ferritin mRNA levels significantly increased in the inulin group. Additionally, the cecal content microflora was examined using 16S ribosomal DNA (rDNA) targeted probes from bacterial DNA. The Lactobacillus and Bifidobacterium populations were significantly increased in the inulin group (P = 0.05) compared to the control group. These results indicate that dietary inulin might trigger an up-regulation of genes encoding for iron transporters in the enterocyte. The specific mechanism for this effect remains to be elucidated.