Effects of iron replenishment on iron, calcium, phosphorus and magnesium metabolism in iron-deficient rats.
We investigated the effect of Fe deficiency on the nutritive utilization of Fe, Ca, P and Mg in rats. Aside from the well known depletion of Fe in liver, femur and sternum with low values of Hb, Fe deficiency impaired Ca, P and Mg metabolism at different degrees. Iron deficiency altered Mg absorption, lowered the concentration of Ca in the liver, femur and sternum, raised the concentration of P and Mg in the liver, and decreased P in the femur. The altered status was not completely rectified by iron supplementation as the animals were still slightly anemic at the end of the study. The second purpose of the study was to evaluate the ability of three iron compounds (ferric citrate, ferrous sulfate and ferrous ascorbate) to correct the undesirable effects of Fe deficiency. Ten days after treatment with these diets, Fe-deficient rats still had reduced Mg absorption, especially those fed ferric citrate. The concentrations of hemoglobin approached normal values in all groups; however, serum Fe remained low, indicating that Fe reserves were still depleted. Hepatic and femoral Fe concentrations were also lower in all Fe-deficient groups regardless of the diet given, compared with their respective controls, whereas Fe concentrations in the sternum increased significantly with all three diets, suggesting an increase in erythropoiesis. The concentration of Ca, P and Mg in liver approached normal values, and appeared to normalize in the femur, except that Ca and P concentrations remained low with the citrate diet. In the sternum, a site assumed to have higher requirements for these minerals, the concentrations of Ca, P and Mg also increased. These findings indicate that Fe is involved in the bone mineralization, and that in physiological terms, Fe interacts favorably with Ca, P and Mg metabolism, since Fe deficiency altered the status of these metals. These findings also suggest that ferrous ascorbate and ferrous sulfate were more effectively absorbed than was ferric citrate.
Pallarés
I
I
Departamento de Fisiología, Facultad de Farmacia, Universidad de Granada, Spain.
López-Aliaga
I
I
Lisbona
F
F
Moratalla
A
A
Gómez-Ayala
A E
AE
Barrionuevo
M
M
Hartiti
S
S
Alférez
M J
MJ
Campos
M S
MS
D000704:Analysis of Variance; D018798:Anemia, Iron-Deficiency / Q000097:blood / Q000188:drug therapy* / Q000378:metabolism; D000821:Animal Feed; D000818:Animals; D001205:Ascorbic Acid / Q000627:therapeutic use; D001835:Body Weight; D002118:Calcium / Q000378:metabolism*; D004435:Eating; D005290:Ferric Compounds / Q000627:therapeutic use; D005296:Ferrous Compounds / Q000627:therapeutic use; D005527:Food, Fortified; D006454:Hemoglobins / Q000032:analysis; D007501:Iron / Q000378:metabolism* / Q000627:therapeutic use; D000090463:Iron Deficiencies; D008274:Magnesium / Q000378:metabolism*; D008297:Male; D010758:Phosphorus / Q000378:metabolism*; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D014018:Tissue Distribution
D005290:Ferric Compounds; D005296:Ferrous Compounds; D006454:Hemoglobins; C051140:iron(II)-ascorbic acid complex; D010758:Phosphorus; C020748:ferrous sulfate; C025314:ferric citrate; D007501:Iron; D008274:Magnesium; D001205:Ascorbic Acid; D002118:Calcium