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Updated: Jun 17, 2026

Quantitating Iron Transport Across the Mouse Placenta In Vivo Using Nonradioactive Iron Isotopes
Published on: May 10, 2022
Difructose anhydride III promotes iron absorption in the rat large intestine
Hiroshi Hara1, Satoshi Onoshima, Chie Nakagawa
1Division of Applied Bioscience, Graduate School of Agriculture, Hokkaido University, Sapporo, Japan. hara@chem.agr.hokudai.ac.jp
Objectives:
We examined the intestinal segment responsible for and the mechanisms involved in the non-digestible disaccharide difructose anhydride III (DFAIII)-mediated enhancement of iron absorption.
Methods:
Net iron and calcium absorption (percentage) were observed in male Sprague-Dawley rats fed an AIN93G-based diet with or without DFAIII (30 g/kg of diet) for 2 wk after cecectomy or laparotomy (experiment 1). The absorption rates of calcium and iron from ligated jejunal loops (experiment 2) or ligated cecal sacs (experiment 3) in anesthetized rats fed a control or DFA diet were observed with or without the addition of DFAIII to the instilled mucosal fluid. Levels of the major iron transporter divalent metal transporter-1 (DMT-1) mRNA per 28S rRNA were evaluated by real-time polymerase chain reaction in the intestinal mucosa.
Results:
Net absorption (percentage) of iron and calcium was higher in the DFA group than in the DFA-free group in laparotomized rats. The enhancement of iron absorption was almost and calcium absorption was partly abolished by cecectomy. The absorption rate of calcium, but not of iron, from the jejunal loops was increased by the addition of DFAIII (100 mmol/L). Iron absorption was clearly higher in the ligated cecal sacs of the DFAIII-fed group than in the DFA-free group with or without the mucosal addition of DFAIII. DMT-1 mRNA level per 28S rRNA was maintained in the cecal mucosa through large increases in cecal size due to DFAIII feeding.
Conclusion:
The DFAIII-induced increases in iron absorption are the result of increased cecal iron absorptive capacity through expansion of the cecal mucosa maintaining DMT-1 mRNA expression.
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