Contribution of Maternal Rat Iron Stores to Fetal Iron in Maternal Iron Deficiency and Overload

Murray, M. J.; Stein, Nell

doi:10.1093/jn/101.11.1583

Cited by 27 publications

(11 citation statements)

References 5 publications

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“…In contrast to previous papers (7,8,19), the maternal tissue iron was markedly lowered at the beginning of gestation in this paper. It appears likely that the more maternal absorbed iron must be required for the normal development of fetus under these conditions, and the subsequent feeding on the iron depleted diet during pregnancy may result in the severe impairment of fetus development.…”

Section: Discussioncontrasting

confidence: 99%

“…Murry and Stein (7) reported that the fetuses obtained more iron from maternal absorption and less from maternal store with diminishing iron store. In contrast to previous papers (7,8,19), the maternal tissue iron was markedly lowered at the beginning of gestation in this paper.…”

Section: Discussionmentioning

confidence: 99%

“…Depletion of iron stores has also been reported to occur at normal pregnancy in the rats due to the transfer of large quantities of iron from maternal stores to the fetus during the final 6 days of gestation (5,6). Murry and Stein indicated that fetus obtained more iron from maternal absorption with diminishing iron stores during pregnancy (7).…”

mentioning

confidence: 99%

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Effect of different intensities of iron-deficient anemia in pregnant rats on maternal tissue iron and fetal development.

Tojyo

1983

Journal of Nutritional Science and Vitaminology, J Nutr Sci Vit

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SummaryEffect of the different intensities of iron-deficient anemia in pregnant rats on the maternal tissue iron and the fetal development was investigated. The different intensities of iron deficiency were produced by changing period of feeding on the iron depleted diet (0.38mg/100g diet) prior to gestation. The anemic rats were divided into three groups with the hemoglobin levels of 12, 10 and 8g/100ml on the first day of gestation. Then, rats of each group were fed on the iron adequate and on the depleted diets during gestation. The whole body weights of the three deficient animals were lower than those of the corresponding controls on day-21 of gestation. Food intakes of the three deficient groups tended to be lower than those of corresponding controls. The values of hemoglobin (Hb), hematocrit (Ht) and red blood cells (RBC) decreased with the progress of pregnancy, and the hypochromic anemia was observed in all deficient animals. Iron contents of various tissues and the ratio of ferritin iron to total iron in liver and spleen of each deficient group were also apparently lower than those of corresponding controls. The numbers of placenta of the deficient groups were similar to those of corresponding controls. The litter size of severe anemic-animals was less than those of light and moderate anemic-animals, and the average body weight of fetus in severe anemic-animals was much lower than those of other groups. These results suggested that a higher severity of anemia in the mother at the beginning of pregnancy may result in a more frequent resorption of the fetus but the anemic status did not affect the ability of gestation itself.

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Section: Discussioncontrasting

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Effect of different intensities of iron-deficient anemia in pregnant rats on maternal tissue iron and fetal development.

Tojyo

1983

Journal of Nutritional Science and Vitaminology, J Nutr Sci Vit

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“…These data are in keeping with previous studies showing that available dietary Fe is di- rected toward the formation of new structures and the maintenance of body weight rather than toward Fe stores [39]. In particular, during pregnancy, the fetus has priority for dietary Fe over maternal stores [40], with more than 70% of dietary Fe being delivered to the fetus toward the end of gestation [41]. We have previously identified some of the mechanisms involved in the placental response to Fe deficiency.…”

Section: Discussionsupporting

confidence: 90%

Effect of Iron Deficiency on Placental Cytokine Expression and Fetal Growth in the Pregnant Rat1

Gambling¹,

Charania²,

Hannah³

et al. 2002

Biology of Reproduction

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Iron deficiency anemia is the most common nutritional disorder in the world. Anemia is especially serious during pregnancy, with deleterious consequences for both the mother and her developing fetus. We have developed a model to investigate the mechanisms whereby fetal growth and development are affected by maternal anemia. Weanling rats were fed a control or iron-deficient diet before and throughout pregnancy and were killed at Day 21. Dams on the deficient diet had lower hematocrits, serum iron concentrations, and liver iron levels. Similar results were recorded in the fetus, except that the degree of deficiency was markedly less, indicating compensation by the placenta. No effect was observed on maternal weight or the number and viability of fetuses. The fetuses from iron-deficient dams, however, were smaller than controls, with higher placental:fetal ratios and relatively smaller livers. Iron deficiency increased levels of tumor necrosis factor alpha (TNFalpha) only in the trophoblast giant cells of the placenta. In contrast, levels of type 1 TNFalpha receptor increased significantly in giant cells, labyrinth, cytotrophoblast, and fetal vessels. Leptin levels increased significantly in labyrinth and marginally (P = 0.054) in trophoblast giant cells. No change was observed in leptin receptor levels in any region of the placentas from iron-deficient dams. The data show that iron deficiency not only has direct effects on iron levels and metabolism but also on other regulators of growth and development, such as placental cytokines, and that these changes may, in part at least, explain the deleterious consequences of maternal iron deficiency during pregnancy.

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“…In cats, maternal transfer of iron in utero principally involves extravasation of maternal erythrocytes into the uterus and is independent of serum iron values [26]. Furthermore, maternal iron supplementation had no effect on milk iron content of lactating rats and iron deficiency in their pups [15,21]. The high iron values observed in queens during lactation further supports the hypothesis that iron deficiency in kittens would not be benefited by maternal supplementation.…”

Section: Discussionmentioning

confidence: 70%

Sequential Changes in Erythrocyte Volume Distribution and Microcytosis Associated with Iron Deficiency in Kittens

Weiser

Kociba

1983

Vet Pathol

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Abstract. Hemograms, erythrocyte volume distribution curves, serum iron and percent transferrin saturation determinations were done on samples from 50 kittens to characterize feline erythrocytic responses between one and ten weeks of age. At one week of age, all kittens had marked macrocytosis and anisocytosis. Most of the macrocytic cells no longer were present by five weeks. Macrocytes were replaced by erythrocytes of normal volume in 30% of the kittens. At five weeks of age, 70%of the kittens had produced microcytic cells which correlated with significantly lower packed cell volume values (p < 0.02) and mean corpuscular volume values (p < 0.00I). Byseven weeks of age, kittens with microcytosis were producing normocytic erythrocytes. Between two and four weeks of age, kittens with microcytosis had significantly lower serum iron and percent transferrin saturation values (p < 0.01) compared to kittens without microcytosis. Between five and seven weeks of age, all kittens had very high iron values which were significantly greater than those of healthy adult cats (p < 0.0 I). Six kittens with low iron values received an iron dextran injection at two to three weeks of age. At five weeks, these kittens had significantly greater mean corpuscular volumes, packed cell volumes (p < 0.0 I) and lower percentage of microcytic cells (p < 0.00I) than littermate controls. These data demonstrate that transient microcytosis and anemia observed in kittens is attributable to iron deficiency. It also was demonstrated that erythrocyte volume distribution curves were more sensitive than the mean corpuscular volume in detecting microcytosis in kittens.Anemia, attributable in part to transient iron deficiency, occurs in the young of numerous species in association with rapid growth rate and all milk diet [I, 6-9, 12, 13, 16,21]. This anemia can be reduced or eliminated by neonatal iron supplementation [6-8, 10, 14-16,21,24]. Hematologic studies in kittens have revealed a mild to moderate normocytic anemia between four and eight weeks of age which slowly disappeared between three and six months of age [2,20]. It was suggested but not documented that the anemia was due to iron deficiency. These studies also indicated that mean corpuscular volume was high at birth and slowly decreased to adult values by about six months of age. No microcytosis was observed. Using sequential erythrocyte size distribution curves (erythrograms), we have observed considerably different changes in erythrocytes. Erythrograms are much more sensitive than mean corpuscular volume values in detecting disturbances of erythrocyte size [3,4,17]. In I

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Contribution of Maternal Rat Iron Stores to Fetal Iron in Maternal Iron Deficiency and Overload

Cited by 27 publications

References 5 publications

Effect of different intensities of iron-deficient anemia in pregnant rats on maternal tissue iron and fetal development.

Effect of different intensities of iron-deficient anemia in pregnant rats on maternal tissue iron and fetal development.

Effect of Iron Deficiency on Placental Cytokine Expression and Fetal Growth in the Pregnant Rat1

Sequential Changes in Erythrocyte Volume Distribution and Microcytosis Associated with Iron Deficiency in Kittens

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