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

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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, P59Fe 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.

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