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Query: UMLS:C0240066 (iron deficiency)
 7,156 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Suprathreshold taste perception and nutrient intake were assessed for two groups of women aged 44 to 56 years: 24 mastectomized breast cancer outpatients and 24 matched controls. Salty and sweet taste intensity and pleasantness were evaluated in aqueous solutions and simple foods by unstructured line scaling. Dietary intakes were assessed by combined dietary recall (1 day) and food record (3 days). Suprathreshold taste intensity and pleasantness data did not differ between the breast cancer and control groups. Breast cancer subjects consumed less energy and were at greater overall nutritional risk than the controls. Compared with control subjects, breast cancer subjects were at greater risk of calcium and iron deficiency. Regression analysis was used to investigate relationships between diet and taste for a breast cancer subgroup (n = 7) with unusually low energy intake (< or = 1,300 kcal/day) and a high overall nutritional risk (25.6%). For the subgroup, significant relationships between taste and diet were found, although taste data did not differ from that of the controls. Percent risks of nutrient deficiency for vitamin B-12, thiamin, folacin, iron, and riboflavin were important predictors of taste-intensity slopes for the cancer subgroup. Findings suggest that for some of the breast cancer subjects, diet may be associated with unsatisfactory nutritional status and may be affected by suprathreshold taste perception.
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PMID:Taste perception and breast cancer: evidence of a role for diet. 831 63

The influence of dietary iron deficiency on acute nickel, lead or cadmium toxicity as reflected by the induction of hepatic, renal and intestinal metallothionein (MT), disposition of the metals, and alterations in hematological parameters was investigated in rats. The administration of cadmium induced the hepatic, renal and intestinal MT while that of nickel or lead induced hepatic MT only. However, dietary iron deficiency did not influence the cadmium induced tissue MT but enhanced the ability of nickel or lead to restore the normal synthesis of renal and intestinal MT lowered under the influence of reduced body iron status. The accumulation of lead in liver and kidney and that of cadmium enhanced in liver only, while tissue deposition of nickel remained unaffected by iron deficiency. The induction of hepatic MT by three metals appears related to the concomitant rise in the hepatic zinc, calcium and iron levels in normal rats. However, dietary iron deficiency increased the hepatic zinc in response to nickel or cadmium and that of heptic calcium in response to lead.
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PMID:Influence of dietary iron deficiency on acute metal intoxication. 835 7

Roots from iron-deficient sugar beet grown in the presence of calcium carbonate exhibit a yellow color and autofluorescence typical of flavin-like compounds, whereas roots of control, iron-sufficient plants exhibited no yellow color and extremely low autofluorescence. The two major flavins whose accumulation is induced by iron deficiency have been shown to be different from riboflavin, FMN, and FAD by reversed-phase high performance liquid chromatography. These flavins, accounting for 82 and 15% of the total flavin concentration in deficient roots, have been shown unequivocally to be riboflavin 3'-sulfate and riboflavin 5'-sulfate, respectively, by electrospray-mass spectrometry, inductively coupled plasma emission spectroscopy, infrared spectrometry, and 1H nuclear magnetic resonance. These flavin sulfates have not been found previously in biological systems. The localization of riboflavin sulfates in deficient roots is similar, but not identical, to that of high iron reductase activity. The concentration of riboflavin sulfates has been estimated from root extracts to be at least 1 mM. We hypothesize, based on the similar localization of flavin and that of iron reduction, that the accumulation of riboflavin sulfates induced by iron deficiency may be an integral part of the turbo iron-reducing system in sugar beet roots.
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PMID:Riboflavin 3'- and 5'-sulfate, two novel flavins accumulating in the roots of iron-deficient sugar beet (Beta vulgaris). 840 31

The purpose of this study was: 1) to establish the prevalence of depleted iron stores, iron deficiency, and low serum levels for copper, zinc, calcium, and magnesium in a healthy female population; and 2) to examine the effects of iron supplementation and discontinuation on the serum levels of the above minerals. One hundred eleven healthy women between the ages of 18 and 40 yr reported for fasted morning blood sampling for iron, copper, zinc, calcium, and magnesium status. Forty-five subjects were either iron-deficient as defined by a hemoglobin level below 120 g.l-1 (four subjects) or iron deplete as defined by a serum ferritin value below 20 micrograms.l-1 (43 subjects). Two subjects fit both criteria. This subgroup continued with the study and were prescribed a normal therapeutic iron dose (320 mg elemental iron per day, taken as two Slow-Fe tablets.d-1 for a period of 12 wk). The subjects then discontinued the iron supplementation for a further 12 wk. The response of the various blood minerals was monitored at 6-wk intervals. Twenty-five subjects completed the full 24-wk treatment. The main conclusions to be made from this study were that: 1) For this sample population of women, iron depletion was quite common (39%), although low hemoglobin values (< 120 g.l-1) were only seen in 3.6%. No subjects fell below the criteria for low serum copper levels (< 13.3 mumol.l-1) nor low serum magnesium levels (< 0.6 mmol.l-1). Seven subjects (6.5%) fell below the criteria for low serum zinc levels (< 11.5 mumol.l-1) while two subjects (1.8%) were below the criteria for low serum calcium levels (< 2.20 mmol.l-1). 2) Therapeutic oral iron supplementation was successful in raising mean serum ferritin values from 15.9 micrograms.l-1 to 36.5 micrograms.l-1 but was not associated with decrements in serum copper or calcium levels. 3) The treatment did not significantly effect serum zinc and magnesium levels during the supplementation period, but a downward trend continued through the discontinuation phase so that at 18 and 24 wk serum zinc and magnesium levels were significantly lower than baseline. 4) Oral contraceptive use was associated with elevated serum copper and ferritin values and lowered serum magnesium levels.
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PMID:Effects of iron supplementation and discontinuation on serum copper, zinc, calcium, and magnesium levels in women. 849 83

The calcium, magnesium and iron intakes provided by food must be sufficient to fulfil the physiological demands of each individual, to avoid the clinical manifestations of mineral deficiencies and to ensure an optimal state of health. For these reasons, it is desirable to ensure a sufficient calcium intake (notably by milk products) at all ages and particularly in children, adolescents and young adults up to the age of 25 (and also in elderly people to prevent osteoporosis); to recommend the consumption of magnesium-rich foods, such a little sifted cereals and dry vegetables to ensure sufficient intakes; to prescribe pharmaceutical preparations on iron systematically in pregnant women and by repeated courses in infants aged 10 to 36 months (to avoid complications due to iron deficiency and notably its harmful influence on haematopoiesis). The consumption of "second age" milks for older children must also be encouraged. Finally, the consumption of foodstuffs with a high vitamin C content should be recommended as it increases the bioavailability of nutritional iron, and the consumption of substances, such as tea and coffee, which inhibit iron absorption must be reduced.
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PMID:[Prevention of mineral deficiencies (iron, calcium and magnesium)]. 850 29

Hypertension (HTN) is a common complication of recombinant erythropoietin (EPO) therapy, but the mechanism of the EPO-associated HTN is uncertain. In the present study we examined the effects of EPO and the vehicle alone on rat caudal artery contractile response and basal and thrombin-stimulated platelet cytosolic Ca2+ concentration ([Ca2+]i) in vitro and on blood pressure (BP) and heart rate in vivo. At high concentrations (200 U/ml) EPO caused a small but consistent contraction in the caudal artery rings (P < 0.01) without affecting the response to either angiotensin II (ANG II) or the alpha 1-agonist methoxamine. Incubation with EPO significantly increased basal platelet [Ca2+]i (P < 0.01) and augmented the thrombin-induced rise of [Ca2+]i in Ca(2+)-free medium (P < 0.05). Long-term EPO administration led to a significant elevation of BP within 2 wk regardless of whether the hematocrit was allowed to rise or was kept constant by dietary iron deficiency. In contrast, single intravenous administration of high-dose EPO (400 and 5,000 U/kg), estimated to yield plasma concentrations comparable with those employed in vitro, failed to either alter BP or modify the BP response to ANG II during a 60-min observation period. This was associated with a significant rise in plasma guanosine 3',5'-cyclic monophosphate but no discernible change in plasma atrial natriuretic peptide, suggesting enhanced nitric oxide (NO) release. Thus, at high concentrations, EPO appears to possess a fast-acting pressor effect in vitro but not in vivo. The observed discrepancy may be due to enhanced NO release with EPO administration in vivo. However, HTN does occur with repeated EPO administration in a time-dependent and hematocrit-independent manner. This suggest that expression of the hypertensive effect of EPO in vivo involves a gradual conditioning process.
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PMID:In vivo and in vitro pressor effects of erythropoietin in rats. 859 78

We studied the mechanism of erythropoietin (EPO)-induced hypertension (HTN) in rats with chronic renal failure (CRF). After partial nephrectomy, rats were randomized into four groups. Group A received EPO, 150 U/kg, two times weekly for 6 wk to prevent anemia; group B received placebo injections and became anemic; group C received EPO but was kept anemic by dietary iron deficiency; and group D received placebo and regular transfusions to match hematocrit (Hct) in group A. Blood pressure (BP), Hct, platelet cytosolic calcium ([Ca2+]i) and magnesium concentration, and pressor and vasodilatory responses were determined. By design, Hct in groups A and D were comparable and significantly greater (P < 0.01) than in groups B and C. Despite divergent Hct values, the EPO-treated groups A and C showed a significant rise in BP compared with the placebo-treated groups B and D. HTN occurred whether EPO therapy was begun immediately or 4 wk after nephrectomy. EPO therapy augmented the elevation of basal [Ca2+]i and restored the defective thrombin-mediated rise of platelet [Ca2+]i in CRF animals. EPO therapy did not alter caudal artery contraction in response to either 68 mM K(+)-induced depolarization, angiotensin II or alpha 1-agonist, methoxamine in vitro, or the pressor response to angiotensin II in vivo. However, EPO therapy impaired the hypotensive response to nitric oxide (NO) donors, sodium nitroprusside and S-nitroso-N-acetyl-D,L-penicillamine, and reversed the CRF-induced upregulation of guanosine 3',5'-cyclic monophosphate production by thoracic aorta in vitro. Thus EPO-induced HTN in CRF rats is Hct independent and is associated with and perhaps causally related to increased basal and stimulated [Ca2+]i and impaired vasodilatory response to NO.
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PMID:Role of nitric oxide resistance in erythropoietin-induced hypertension in rats with chronic renal failure. 876 88

1. Our aim was to investigate the effect of experimental iron deficiency on cardiac functional properties. We recorded ventricular isometric twitch, action potentials and the L-type Ca2+ current in isolate ventricular myocytes from iron-deficient rats and control rats. 2. Twitch tension and maximal rates of tension activation and relaxation were reduced in iron-deficient compared with control rats, whereas twitch duration was prolonged. Isoproterenol (10-(6) mol/l) augmented tension in iron-deficient rats (P < 0.05), but only moderately affected control rats. In contrast, maximal rates of tension activation and relaxation were increased equally by isoproterenol in the two groups. 3. To determine the mechanism(s) responsible for the reduced mechanical function in iron-deficient rats, action potentials and the L-type Ca2+ current (with or without isoproterenol) were recorded in both groups. 4. The L-type Ca2+ current was smaller in ventricular myocytes from control rats than in those from iron-deficient rats; at a membrane potential of 0 mV, L-type Ca2+ current amplitudes were -1.44 +/- 0.18 and -0.97 +/- 0.07 nA in myocytes from control and iron-deficient rats respectively (P < 0.05). 5. Action potential duration was markedly shortened in myocytes from iron-deficient compared with control rats; action potential duration at 50% repolarization was 12.0 +/- 1.6 and 7.2 +/- 1.4 ms in myocytes from control and iron-deficient rats respectively (P < 0.01). These iron deficiency-induced electrophysiological alterations most probably contribute to the depressed mechanical function in iron-deficient rats. 6. The L-type Ca2+ current was augmented equally by isoproterenol in the two groups, suggesting that the enhanced inotropic responsiveness in iron-deficient rats was not due to an increased response of the L-type Ca2+ current. 7. These results may have an important implication for anaemic (iron-deficient) patients; the attenuation of their cardiac mechanical performance may be compensated by an increased reactivity to beta-adrenergic stimulation.
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PMID:Experimental iron deficiency in rats: mechanical and electrophysiological alterations in the cardiac muscle. 879 49

One objective of this clinical trial was to determine whether calcium and phosphorus supplementation of infant formula affects the iron status of healthy full-term infants. One hundred three infants were randomly assigned to receive iron-fortified, cow milk-based infant formula (465 mg Ca and 317 mg P/L) or the same formula with added calcium glycerophosphate (1800 mg Ca and 1390 mg P/L) for 9 mo. Reported calcium intake for supplemented infants was about four times that of control infants, ranging from a mean of 1741 mg/d at baseline to 1563 mg/d at 9 mo. There was no difference by treatment group in mean or median change from baseline of serum ferritin, total-iron-binding capacity, erythrocyte protoporphyrin, or hematocrit at 4 and 9 mo after enrollment. Incidence of iron deficiency was similar for both groups and no infant developed iron deficiency anemia during the trial. This study indicates that the well-documented inhibitory effect of calcium and phosphorus on iron absorption is not clinically important in infants fed iron-fortified infant formula.
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PMID:Calcium and phosphorus supplementation of iron-fortified infant formula: no effect on iron status of healthy full-term infants. 909 73

We studied the effects of iron deficiency on the in vivo absorption (by using the intestinal perfusion technique in the duodenum) of different dietary sources of iron (haem, non-haem and equal parts of both forms) and investigated the interactions between iron and calcium, phosphorous, magnesium, copper and zinc in control and iron-deficient rats. Three perfusion solutions containing a different source of iron were used: solution 1, ferric citrate; solution 2, haemoglobin; solution 3, equal parts of ferric citrate and haemoglobin. We also tested the same perfusion solution with 2,4-dinitrophenol (2,4-DNP), an inhibitor or oxidative phosphorylation (solutions 1-I, 2-I and 3-I). In control rats we observed three mechanisms of iron absorption: passive for soluble iron salts, active receptor-mediated for non-haem iron complexes, and active receptor-mediated for haem iron. In anaemic rats iron absorption was greater than in controls, except after perfusion with solution 2 (containing haemoglobin). Absorption increased as a result of both the passive and active, receptor-mediated mechanism for non-haem iron complexes. The active component was influenced by the depletion of haem receptors under severe iron deficiency. The absorption of calcium, copper and zinc in iron-deficient animals was lower than in controls, whereas phosphorus and magnesium absorption were not significantly affected. After perfusion with solution 2 or 3, calcium, copper and zinc absorption were lower than after solution 1. We conclude that ferropoenic anaemia in the rat impairs the absorptive process of those minerals that are absorbed, at the duodenal level mainly via active transport (haem iron, calcium, copper and zinc), but does not affect the active component involved in non-haem iron absorption.
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PMID:Effect of source of iron on duodenal absorption of iron, calcium, phosphorous, magnesium, copper and zinc in rats with ferropoenic anaemia. 912 53


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