Mechanism underlying the inhibitory effect of high calcium carbonate intake on iron bioavailability from ferrous sulphate in anaemic rats

Abstract

The influence of high CaCO3, intake on the bioavailability of Fe from FeSO4, was assessed during Fe repletion of rats with Fe-deficiency-induced anaemia. Fe-deficient rats with a mean blood haemoglobin concentration of 4. 1 mmol/l were fed on purified Fe-adequate diets containing either 6.2 or 25.0g CaCO,/kg (ten rats per group). Haemoglobin repletion after 14 d was significantly depressed by high CaCO, intake (9.5 v. 9.8 mmol/l for high and low CaCO, intake respectively; P = 0·03), as was apparent Fe retention (367 v. 552 µg/d during days 5–7, P<0·001; 146 v. 196 µg/d during days 19–21, P < 0·001). The concentration of Fe in the liquid phase of the proximal half of the small intestine was significantly lower in the high-CaCO, group (3.71 v. 520 µg/g digesta; P = 0-02). Mucosal uptake and mucosal transfer of Fe were determined with orally administered59Fe and Cr as a non-absorbable marker. Mucosal transfer was significantly diminished by CaCO, loading (90 v. 100% of mucosal uptake; P = 0·04), whereas mucosal uptake was not.59Fe retention values at 14 d after administration were not significantly different (57.6 v. 51.9%; P = 0·14). Fe contents of liver and spleen were significantly decreased by high compared with low CaCO, intake (879 v. 590 pg Fe in liver, P < 0·001; 92 v. 63pg Fe in spleen, P <0·001). It is concluded that high intake of CaCO, depresses Fe bioavailability in rats. The CaCO,-induced decrease in Fe solubility in the digesta probably was associated with an increased efficiency of mucosal Fe uptake so that the amount of mucosal uptake remained unaltered. The CaCO,-induced decrease in Fe transfer through the mucosal cytoplasm and/or basolateral membrane may have been responsible for the concurrent decrease in Fe bioavailability.