An iron-fortified whey protein concentrate (Fe-WPC) was prepared by addition of ferric chloride to concentrated whey. A large part of the iron in the Fe-WPC existed as complexes with proteins such as ${\beta}$-lactoglobulin. The bioavailability of iron from Fe-WPC was evaluated using iron-deficient rats, in comparison with heme iron. Rats were separated into a control group and an iron-deficiency group. Rats in the control group were given the standard diet containing ferrous sulfate as the source of iron throughout the experimental feeding period. Rats in the iron-deficiency group were made anemic by feeding on an Fe-deficient diet without any added iron for 3 wk. After the iron-deficiency period, the iron-deficiency group was separated into an Fe-WPC group and a heme iron group fed Fe-WPC and hemin as the sole source of iron, respectively. The hemoglobin content, iron content in liver, hemoglobin regeneration efficiency (HRE) and apparent iron absorption rate were examined when iron-deficient rats were fed either Fe-WPC or hemin as the sole source of iron for 20 d. Hemoglobin content was significantly higher in the rats fed the Fe-WPC diet than in rats fed the hemin diet. HRE in rats fed the Fe-WPC diet was significantly higher than in rats fed the hemin diet. The apparent iron absorption rate in rats fed the Fe-WPC diet tended to be higher than in rats fed the hemin diet (p = 0.054). The solubility of iron in the small intestine of rats at 2.5 h after ingestion of the Fe-WPC diet was approximately twice that of rats fed the hemin diet. These results indicated that the iron bioavailability of Fe-WPC was higher than that of hemin, which seemed due, in part, to the different iron solubility in the intestine.
Iron deficiency is a severe nutritional problem in the world. Coffee intake of the people is increasing every year and it can increase the loss of several essential body minerals including iron. Either iron deficiency or coffee intake may increase the oxidative stress of the body. However, the effect of iron deficiency and/or coffee intake on peroxidation have not been studied much. Therefore, the aim of this study was to investigate the effect of coffee intake on oxidative stress and antioxidative enzyme activities of iron-deficient rats. Forty-eight male rats of Sprague-Dawley strain were divided into two groups by dietary iron levels. Iron deficient group were fed 5 ppm iron diet and iron-sufficient group were fed 50 ppm iron diet. Each iron group were divided into three sub-groups by coffee levels (0%, 1%, 4%) included in the experimental diet. The experimental diets were fed for 4 weeks. The hemoglobin level was significantly low in iron deficient group and the level was exacerbated by high coffee intake. The malondialdehyde concentration of the plasma and liver were not affected by iron or coffee level in this study. However, plasma aspartate aminotransferase and alanine aminotransferase, the indicator of the liver damage, were increased by high coffee intake. The erythrocyte and liver superoxide dismutase (SOD) activities were elevated in iron deficient groups. Coffee intake increased erythrocyte SOD activity in iron sufficient groups. Glutathione peroxidase and catalase activities were not influenced much by either iron or coffee intake. In conclusion, high coffee intake in iron deficiency may not only increase the anemia symptoms, but also may increase the oxidative stress of the body.(Korean J Nutrition 35(9) : 919~925, 2002)
BACKGROUND/OBJECTIVES: Iron deficiency in early life is associated with developmental problems, which may persist until later in life. The question of whether iron repletion after developmental iron deficiency could restore iron homeostasis is not well characterized. In the present study, we investigated the changes of iron transporters after iron depletion during the gestational-neonatal period and iron repletion during the post-weaning period. MATERIALS/METHODS: Pregnant rats were provided iron-deficient (< 6 ppm Fe) or control (36 ppm Fe) diets from gestational day 2. At weaning, pups from iron-deficient dams were fed either iron-deficient (ID group) or control (IDR group) diets for 4 week. Pups from control dams were continued to be fed with the control diet throughout the study period (CON). RESULTS: Compared to the CON, ID rats had significantly lower hemoglobin and hematocrits in the blood and significantly lower tissue iron in the liver and spleen. Hepatic hepcidin and BMP6 mRNA levels were also strongly down-regulated in the ID group. Developmental iron deficiency significantly increased iron transporters divalent metal transporter 1 (DMT1) and ferroportin (FPN) in the duodenum, but decreased DMT1 in the liver. Dietary iron repletion restored the levels of hemoglobin and hematocrit to a normal range, but the tissue iron levels and hepatic hepcidin mRNA levels were significantly lower than those in the CON group. Both FPN and DMT1 protein levels in the liver and in the duodenum were not different between the IDR and the CON. By contrast, DMT1 in the spleen was significantly lower in the IDR, compared to the CON. The splenic FPN was also decreased in the IDR more than in the CON, although the difference did not reach statistical significance. CONCLUSIONS: Our findings demonstrate that iron transporter proteins in the duodenum, liver and spleen are differentially regulated during developmental iron deficiency. Also, post-weaning iron repletion efficiently restores iron transporters in the duodenum and the liver but not in the spleen, which suggests that early-life iron deficiency may cause long term abnormalities in iron recycling from the spleen.
Iron deficiency affects approximately one-third of the world's population, occurring most frequently in children aged 6 months to 3 years. Mechanisms of iron absorption are similar to those of other divalent metals, particularly manganese, lead, and cadmium, and a diet deficient in iron can lead to excess absorption of manganese, lead, and cadmium. Iron deficiency may lead to cognitive impairments resulting from the deficiency itself or from increased metal concentrations caused by the deficiency. Iron deficiency combined with increased manganese or lead concentrations may further affect neurodevelopment. We recently showed that blood manganese and lead concentrations are elevated among iron-deficient infants. Increased blood manganese and lead levels are likely associated with prolonged breast-feeding, which is also a risk factor for iron deficiency. Thus, babies who are breast-fed for prolonged periods should be given plain, iron-fortified cereals or other good sources of dietary iron.
Journal of the Korean Society of Food Science and Nutrition
/
v.28
no.3
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pp.705-709
/
1999
To evaluate iron bioavailability in iron fortified milk, in vitro and in vivo method were used. Low molecular weight components(ILC) from milk was isolated and iron was added, then soluble iron from ILC iron complex was determined. Each iron sources and extrinsically labelled with FeCl3 was used for measuring absorption rate of iron from ILC radiolabelled iron complexes as radioiron absorption into the blood one hour after injection into ligated duodenal loops of iron deficient rats. Iron absorption rate was in the order of ferrous lactate(25.56%)$\geq$ferric citrate(24.71%)$\geq$ferrous sulfate(19.67%) when 100ppm iron was used. In separate experiments, iron fortified milks with each iron sources were gavaged into iron deficient rats. When 25ppm iron was added to milk, the order of iron absorption was ferrous sulfate(12.52%)>ferrous lactate(8.07%)>ferric citrate(6.52%) (p<0.05). When 100ppm iron was added to milk, absorption rate was decreased compared to the treatments with added 25ppm of iron. Absorption rate of ferrous sulfate(5.34%) from milk added 100ppm iron was highly lowered, but ferric citrate(6.45%) was not significantly changed. The absorption rate of ferrous lactate(5.82%) was 70% of 25ppm iron added milk.
The purpose of this research is to assess th iron nutritional status of pregnant women and to evaluate the appropriateness of the present cut off levels of hemoglobin(Hgb), hematocrit(Hct) and total iron binding capacity(TIBC) for assessing iron deficiency status. Pregnant women who were visiting public helath centers in Ulsan were interviewed and agreed to attend the study. Blood sample was taken and biochemical analysis of blood was performed. The collected data were classified into 3 trimesters by gestational age and then statistical analysis was performed. The prevalence of anemia in all subjects was 32.3% by WHO criteria(Hgb < 11.0g/dl) and 17.8% of all subjects was iron deficient anemia by CDC criteria(Hgb < 11.0/dl and serum ferritin < 12.0ug/l). Since the iron deficient anemia generally occures at the last stage of iron deficiency, it is not efficient to diagnose and prevent the iron deficient anemia in pregnant women by using the present cut off level of Hgb. Therefore, the new cut off level of iron status indices is necessary for assessing iron deficiency in early pregnancy before manifestation of anemia and for reducing the prevalence of anemia in later pregnancy. For this reason, the present cut off levels of iron status indices were estimated and compared by assessing the iron deficiency judged by serum ferritin level (<12.0ug/l)as true iron deficiency. It follows from the results of this research that present cut off levels of Hgb, Hct and TIBC were very insensitive in identifying the subjection with iron deficiency. The appropriate cut off levels of Hgb were 11.5g/dl for total period of pregnancy, 12.0g/dl for 1st and 3rd trimester, and 11.5g/dl for 2nd trimester. The cut off level of Hct was 34.0% for total period for pregnancy, 35.0% for 1st trimester, and 34.0% for 2nd and 3rd trimester. The cut off level of TIBC was 400ug/dl for total period, 360ug/dl for 1st 2nd trimester, and 450ug/dl for 3rd trimester.
This study examined the effect of excess loading of calcium (Ca)and iron(Fe) on the bioavailability of minerals in both normal and Ca-and Fe-deficient rats. Three-week-old male rats were divided into four groups and fed experimental diets for six weeks, containing either normal (0.5%) or high(1.5%) Ca and normal (35ppm) or high (350ppm)Fe. Likewise, three-week-old male rats were first fed a Ca-and Fe-deficient diet for three weeks, and then fed one of four experimental diets for additional three weeks. In both normal and Ca-and Fe-deficient rats, ca contents of serum, liver, kidney and femur were not significantly affected by dietary Ca and Fe levels. Apparent Ca absorption(%) decreased in rats fed a high Ca diet regardless of dietary Fe levels. Magnesium(Mg) contents of serum, liver and femur significantly decreased in rats fed a high Ca diet. Fe contents of serum and liver significantly increased in rats fed a high-Fe diet, but decreased in rats fed a high Ca diet. Fe content of serum and liver significantly increased in rate fed a high-Fe diet, decreased in rats fed a high-Ca diet. Apparent Fe absorption increased in rats fed a high-Fe diet, and decreased in rats fed a high-Ca diet in Ca-and Fe-deficient rats, but dietary Ca did not seem to affect Fe absorption in normal rats. Phosphorus(P) contents of serum and femur were not significantly affected by dietary Ca and Fe levels in both normal and Ca-and Fe-deficient rats. Serum copper(Cu) decreased in rats fed a high-Fe diet, while serum zinc(Zn) decreased in rats fed a high-Ca diet in normal rats. Cu contents of liver, and Zn contents of serum and liver decreased in rats fed a high-Fe diet in Ca-and Fe-deficient rats. There results suggest that a dietary overload of Ca and Fe in both normal and Ca-and Fe-deficient rats may decrease mineral bioavailability leading to potential health problems.
This study examined the effect of excess calcium (Ca) on the iron (Fe) bioavailability and bone growth of marginally Fe deficient animals. Two groups of weanling female SD rats were fed either normal Fe (35 ppm) or Fe deficient diet (8 ppm) for 3 weeks. Then each group of animals were assigned randomly to one of three groups and were fed one of six experimental diets additionally for 4 weeks, containing normal (35 ppm) or low (15 ppm) Fe and one of three levels of Ca as normal (0.5%), high (1.0%), or excess (1.5%). Feces and urine were collected during the last 3 days of treatment. After sacrifice blood, organs, and femur bone were collected for analysis. Final body weight and average food intake were not affected by either the levels of dietary Ca or Fe. Low Fe diet significantly reduced the level of serum ferritin, however, for Hb, Hct, and TIBC no difference was shown than those in the normal Fe group. TIBC increased slightly by high and excess Ca intake in low Fe groups. For both normal and low Fe groups, high and excess Ca intakes reduced the apparent absorption of Fe and Fe contents of liver significantly (p < 0.05). Calcium contents in kidney and Femur of rats that were fed high and excess levels of Ca were significantly greater than those of normal Ca groups. However, weight, length, and breaking force of the bone were not affected by increased Ca intakes. Both in control and low Fe groups, high and excess intakes of Ca decreased the apparent absorption of Ca. These results indicate that the excess intakes of calcium than the normal needs would be undesirable for Fe bioavailability and that the adverse effects be more serious in marginally iron deficient growing animals. In addition bone growth and strength would not be favorably affected by high Ca intakes, though, the long term effect of increased Ca contents in bone requires further examination.
Journal of the Korean Society of Food Science and Nutrition
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v.40
no.12
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pp.1720-1725
/
2011
Aspartic acid chelated iron (Asp-Fe) was synthesized by a new method using calcium carbonate, aspartic acid, and ferrous sulfate. This study was carried out to investigate the bioavailability of Asp-Fe in iron-deficient rats. We divided the rats into four experimental groups. The first was the normal diet control group, or NC. The second was the no treated control group of iron-deficient (ID) rats, or ID+C. The third was the heme-iron (heme-Fe) treated group of ID rats, ID+heme-Fe. And the fourth was the Asp-Fe treated group of ID rats, or ID+Asp-Fe. There were no differences among any of the experimental groups in diet consumption, change of body weight, or the weight of the livers, kidneys, or spleens. After 7 days of feeding, the iron content in the sera of the ID+Asp-Fe group (175.2 ${\mu}g$/dL) and the ID+heme-Fe group (140.8 ${\mu}g$/dL) were significantly higher than that of the ID-C group (96.1 ${\mu}g$/dL). The total iron binding capacity (TIBC) of the ID+Asp-Fe group (735.4 ${\mu}g$/dL) was significantly normalized compared to the ID+C group (841.9 ${\mu}g$/dL) or ID+heme-Fe group (824.6 ${\mu}g$/dL). The hematocrit level of the ID+Asp-Fe group was increased to normal levels, but there was no statistical difference among ID groups. The absorption ratio of heme-Fe was 21.3% and that of Asp-Fe was 50.2%, which indicates a 2.3 times higher ratio in comparison with heme iron. With the above results we found that Asp-Fe seems to be an efficient form of iron to supply iron deficient rats in order to cure them of anemia. Thus, these findings suggest that aspartic acid chelated iron has the potential to serve as a functional food related to iron metabolism.
Chlorella ellipsoidea cells were cultured in an iron, copper, zinc, manganese, molybdenum or boron-free medium. Physiological activities such as growth rate, reproduction, endogenous and glucose respiration, photosynthetic activity and biosythesis of chlorophyll of the micro-element definition cells were measured. It generally, growth rate, respiratory and photosynthetic activities, and biosynthesis of chlorophyll of the micro-element deficient cells decreased more or less, compared with those of the normal cells. The growth of the algal cells in an iron-free medium were retarded severely with the chlorosis, and the photosynthetic activity of the cells decreased remarkably even though the low content of chlorophyll in the cells owing to the iron-deficiency is considered. Therefore, it is deduced that iron takes part in the photosynthetic process itself, possibly by its participation in the photo phosphorylation coupled with electron transport. Respiratory activity of boron-deficient cells showed the most severe decrease whereas those of the molybdenum-deficient cells showed very slight decrease in spite of severe growth retardation.
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