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

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 25.0 g CaCO3/kg (ten rats per group). Haemoglobin repletion after 14 d was significantly depressed by high CaCO3 intake (9.5 v. 9.8 mmol/l for high and low CaCO3 intake respectively; P = 0.03), as was apparent Fe retention (367 v. 552 micrograms/d during days 5-7, P < 0.001; 146 v. 196 micrograms/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-CaCO3 group (3.71 v. 5.20 micrograms/g digesta; P = 0.02). Mucosal uptake and mucosal transfer of Fe were determined with orally administered 59Fe and Cr as a non-absorbable marker. Mucosal transfer was significantly diminished by CaCO3 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 CaCO3 intake (879 v. 590 micrograms Fe in liver, P < 0.001; 92 v. 63 micrograms Fe in spleen, P < 0.001). It is concluded that high intake of CaCO3 depresses Fe bioavailability in rats. The CaCO3-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 CaCO3-induced decrease in Fe transfer through the mucosal cytoplasm and/or basolateral membrane may have been responsible for the concurrent decrease in Fe bioavailability.