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

During the past 20 years there have been great developments in the scientific understanding of the role of nutrition in health and physical performance. Epidemiological and physiological studies have provided evidence that certain forms of dietary behaviour may be linked with an increased risk of developing disorders such as high blood pressure, coronary artery disease and some cancers. This has resulted in dietary recommendations that are intended to reduce the incidence of these disorders in the community. The science of nutrition in relation to sports performance has progressed from empirical studies investigating the effects of dietary manipulations, such as restriction and supplementation, to the direct investigation of the physiological basis of the specific nutritional demands of hard physical exercise. This review is based on the premise that it is "what comes out' rather than "what goes in', which provides the clues to ideal nutrition for athletic performance. Various aspects of the physical demands of athletic exercise are viewed as stresses that induce specific biochemical, and hence nutritional, strains in the athlete. Training is the predominant demand in the athletic lifestyle. This is characterised by acute bouts of high power output. During one hour of hard training an athlete may expend 30% of his or her total 24-hour energy output. These high power outputs have important implications for energy substrate and water requirements. Carbohydrate, specifically muscle glycogen, is an obligatory fuel for the high power outputs demanded by athletic sports. Muscle glycogen is a limiting factor in hard exercise because it is held in limited amounts, utilised rapidly by intense exercise, and fatigue occurs when it is depleted to low levels in the active muscles. Liver glycogen may also be exhausted by hard exercise and low blood glucose contributes to fatigue. High sweat rates are demanded during severe exercise and large water deficits commensurate with energy expenditure are incurred during extended periods of hard training and competition. Salt, potassium, and magnesium are lost in nutritionally significant amounts in the sweat, but vitamins and trace elements are not. Adaptive mechanisms protect athletes against electrolyte depletion. Iron loss in sweat may contribute to the iron deficiency seen in some endurance runners. Protein is degraded and amino acids are oxidised during physical exercise. Protein is also retained during muscle building training. Recent investigations indicate that the minimal protein requirements of athletes may be substantially higher than those for sedentary persons.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Nutrition and sports performance. 639 Jun 9

Studies of red cell metabolism, erythropoeitin concentration, iron and folate status were made in 48 children with protein-energy malnutrition in Johannesburg (altitude 1800 m). Biochemical evidence of iron deficiency was presented in 26% cases on admission and developed in 90% during recovery. Biochemical evidence of folate deficiency was present in 14% of cases on admission and resolved on dietary therapy alone. Serum erythropoeitin was increased on admission and remained elevated during recovery. There was no relationship between serum erythropoeitin and Hb concentrations. Key enzymes in the red cell glycolytic and hexose monophosphate pathways and red cell membrane showed increased activity. Red cell adenosine triphosphate concentration was increased and unstable. Red cell potassium was decreased and, in the fatal cases, red cell sodium was increased. The possible significance and practical implications of these findings are discussed.
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PMID:Mechanisms of anemia in protein-energy malnutrition in Johannesburg. 646 Dec 44

The effect of iron-deficiency anaemia and iron supplementation on the enzyme profile and conversion of specifically labelled glucose to 14CO2 and 14C-lipid was measured in rat adrenal glands. Enzymes involved in lipogenesis were severely depressed in iron deficiency, addition of Fe2+ to the diet resulted in increased activity of fatty acid synthetase (+75%), NADP isocitrate dehydrogenase (+466%), glucose-6-phosphate dehydrogenase (+27%) and malic enzyme (+46%). Parallel increases occurred in the flux of glucose into lipid. The effects of iron-deficiency anaemia on adrenal and thyroid function in relation to developmental processes are discussed.
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PMID:Bio-inorganic regulation of pathways of carbohydrate and lipid metabolism. II. The effect of iron-deficiency on the profile of enzymes in the developing rat adrenal gland. 707 81

The effects of chronic iron deficiency anemia on brain (cortex) metabolism were estimated by 31P-nuclear magnetic resonance spectroscopy and biochemical analyses in male Wistar rats. Iron deficiency anemia was induced by supplying diet containing either approximately 2 or approximately 6 ppm Fe. Control diet was supplemented with 100 ppm Fe as ferric citrate. After 8-9 weeks, blood hemoglobin levels were approximately 13, 5, and 3 g/100 ml in the 100 ppm, 6 ppm, and 2 ppm Fe group, respectively. The blood lactate levels at rest in these groups were approximately 3, 5, and 6 mM. The blood glucose concentration also tended to be elevated in iron-deficient rats. The high-energy phosphate contents in brain were not affected by iron deficiency. The activities of succinate dehydrogenase and cytochrome oxidase per unit protein in the 2 ppm Fe group were significantly less than in the 100 ppm Fe group, but those activities were not significantly affected by feeding diet with 6 ppm Fe. The activities of lactate dehydrogenase in iron-deficient group tended to be elevated but not significantly. The activities of non-iron containing mitochondrial enzymes, citrate synthase and beta-hydroxyacyl CoA dehydrogenase, were unchanged. It is suggested that the brain has a higher tolerance to iron deficiency than skeletal muscle in terms of the metabolic characteristics, although this may be associated with a lower level of neural activity.
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PMID:Effects of chronic iron deficiency anemia on brain metabolism. 756 62

We have studied the prevalence and molecular nature of hereditary anaemias (abnormal haemoglobins, beta-thalassaemia, alpha-thalassaemia, and Glucose 6 phosphate dehydrogenase (G6PD) deficiency) in a primitive central Indian tribe, the Baiga. 43% of the population appear to be iron-deficient. Hereditary anaemia gene frequencies are, sickle cell 0.0824, G6PD deficiency (in males) 0.0457, beta-thalassaemia 0.0057, and deletional alpha-plus thalassaemia 0.65. Both -alpha 3.7 and -alpha 4.2 deletions were observed and non-deletional alpha-thalassaemia was suspected. The overall gene frequency of Xmn I+polymorphism (C-->T - 158 cap site; upstream of G gamma region) is 0.35. This polymorphism is preferentially linked to beta s genes. It appears that sickle cell disease covers a wide range of severity in the Baiga tribe based on higher mortality in the offspring of AS x AS parents (2.5/couple) compared to AA x AS (0.75/couple) and AA x AA (0.76/couple) parents. This is compatible with the high frequency of genetic modifying factors, i.e., the Xmn I polymorphism and alpha-thalassaemia. The results also indicate that "normal" red cell values must be defined for each population where thalassaemias, G6PD deficiency and iron deficiency are common.
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PMID:Hereditary anaemias and iron deficiency in a tribal population (the Baiga) of central India. 762 84

To evaluate the hypothesis that mild iron deficiency increases dependence upon gluconeogenesis, control and mildly iron-deficient (Hb = 80 +/- 2 g/L) rats were injected with mercaptopicolinic acid (MPA), a known inhibitor of gluconeogenesis, or with injection vehicle (sham) and studied at rest or after 30 min of treadmill running (13.4 m/min, 0% grade). Liver glycogen concentration was lower in resting iron-deficient rats than in resting control rats, but iron deficiency did not influence arterial substrates or hormones in sham-treated rats. Glucose and insulin concentrations were less in resting control and iron-deficient MPA-treated rats than in sham-treated animals. However, arterial lactate was greater in resting iron-deficient MPA-treated rats than control MPA-treated animals, and glucagon and epinephrine were greater in resting iron-deficient MPA-treated rats than in iron-deficient sham-treated animals, indicating that gluconeogenesis is more important to maintenance of euglycemia in resting iron-deficient animals than in controls. Moderate exercise stimulated glucose metabolism in iron-deficient rats, as evidenced by the lower arterial glucose and higher arterial lactate when compared with resting iron-deficient rats. However, MPA treatment did not clearly establish differences between iron-deficient and control rats after exercise. Therefore, changes in substrate and hormone concentrations in resting iron-deficient MPA-treated rats indicate that dependence on gluconeogenesis for maintenance of euglycemia is greater at rest with dietary iron deficiency. Furthermore, consistent with previously published results for severely iron-deficient rats, results from the present investigation indicate that dependence on glucose metabolism is greater during moderate exercise in mildly iron-deficient rats.
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PMID:Maintenance of euglycemia is impaired in gluconeogenesis-inhibited iron-deficient rats at rest and during exercise. 796 96

To evaluate the hypothesis that lactate supply is essential to maintain euglycemia during iron deficiency, female Sprague-Dawley rats were assigned to iron-sufficient (50 mg Fe2+/kg diet, +Fe), or iron-deficient (15 mg Fe2+/kg diet, -Fe) dietary groups and were injected with a specific beta 2-adrenergic inhibitor, ICI 118,551 (1.0 mg/kg body wt). Rats were studied at rest or after 30 min of running at 13.4 m/min 0% grade. Dietary iron deficiency decreased hemoglobin concentration 38%, but resting arterial concentrations of glucose ([Glc]), lactate ([La]), or alanine ([Ala]) were unaffected. Administration of ICI 118,551 (beta 2-blockade) decreased [La] and [Glc] 52 and 32% in resting -Fe rats, respectively. beta 2-Blockade attenuated the exercise-induced rise in [La] and decreased [Glc] 31% in exercising -Fe rats. [Ala] were unaffected by iron deficiency or exercise but decreased 24 and 18% because of beta 2-blockade in resting and exercising +Fe rats. Iron deficiency depleted resting liver glycogen concentration 45%, with no additional effect of exercise or beta 2-blockade. beta-Blockade decreased arterial insulin and increased arterial glucagon concentrations in resting -Fe and +Fe rats. During exercise glucagon concentration increased significantly more in -Fe than +Fe rats. Decreased arterial [La] with a corresponding decrease in arterial [Glc] in response to beta 2-blockade support the contention that lactate supply is critical to maintenance of euglycemia in -Fe rats at rest and during exercise.
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PMID:Lactate is essential for maintenance of euglycemia in iron-deficient rats at rest and during exercise. 809 76

A case of posttransplant erythrocytosis in a 51-year-old diabetic man is described. This problem, which can occur in 5 to 15% of renal transplant patients, can result from a contracted plasma volume (diuretics, pressure natriuresis, or glycosuria) or from a true elevation in red blood cell mass. Once the diagnosis of true erythrocytosis is made by a radiolabeled red blood cell mass study, secondary causes such as hypoxia, liver disease, polycythemia rubra vera, renal artery stenosis, and cystic kidney disease should be excluded. Posttransplant erythrocytosis has only been observed in renal transplant recipients and appears to be more frequent with cyclosporine compared with azathioprine therapy. An inappropriately high level of erythropoietin has been described in some, but not all patients, suggesting stimulation of erythropoietin production as the mechanism. Posttransplant erythrocytosis can be associated with an increased incidence of thrombotic events. The presence of this potential complication has prompted intervention to maintain the hematocrit below 50 to 55%. Measures such as discontinuation of diuretics as well as better control of blood pressure and plasma glucose should be used to facilitate the correction of extracellular volume contraction. Phlebotomy has been the most accepted intervention to intermittently lower the hematocrit when needed, but this can lead to iron deficiency. Newer therapeutic modalities are now being used to treat the problem medically. Theophylline, which reduces adenosine-mediated erythropoietin synthesis, is effective but may be associated with side effects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Posttransplant erythrocytosis: case report and review of newer treatment modalities. 831 81

The subchronic toxicity following dermal exposure to a synthetic fuel, heavy gas oil No. 2 fraction of bitumen upgrading product (B-HGO II) was studied in the rat. B-HGO II was applied on the dorsal skin of rats at doses of 8, 20, 50 and 125 mg/kg bw/day daily for 13 weeks. Control animals received normal saline and positive controls received a medium-boiling coal liquefaction product (CLP) at 125 mg/kg bw/day. Both male and female rats in the treatment groups had reduced body weight gain, and males in the highest dose group were terminated in the 5th week due to overt toxicity. Increased liver weight relative to body weight was observed in males and females starting at 8 mg/kg. Increased relative heart and spleen weights were observed in males and females starting at the two intermediate doses (20, 50 mg/kg). Increased relative kidney weight was detected in males at 50 mg/kg and females at 125 mg/kg. Increased serum cholesterol was observed in both sexes starting at 50 mg/kg while elevated serum glucose was present in females starting at 8 mg/kg. Significant changes in AH, APDM and EROD activities were observed in treated rats of both sexes. Reduced red blood cell counts were detected in males starting at 8 mg/kg and females at 20 mg/kg. Microscopic examination of blood smears, spleen and hemosiderin accumulation patterns, as well as analysis of FEP and serum TIBC levels indicated that the cause of anemia was primarily intravascular hemolysis and secondarily iron deficiency. Marked thymic atrophy and thyroid abnormalities were the most prominent histological changes followed by changes in bone marrow (myelofibrosis) and liver. Both B-HGO II and CLP (positive control) caused kidney changes characterized by cytoplasmic inclusions and lesions in the tubular cells, which were observed in 50 mg/kg males but not in the females. B-HGO II was considered to be toxic at a subchronic dermal exposure level as low as 8 mg/kg/day.
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PMID:Systemic toxicity of a bitumen upgrading product in the rat following subchronic dermal exposure. 865 44

An increasing number of mice with genetic variation of intestinal transfer properties is becoming available. A luminal perfusion system for small intestinal segments, therefore, was adapted for the use in mice and rat pups to investigate longitudinal differences in intestinal drug and toxin transfer and to explore the adaptation of transfer properties during maturation under standardized conditions in vitro. At present, cell cultures are inadequate for this goal. The perfusator consists of an upper reservoir and a lower moist chamber to accommodate the intestinal segment. The luminal perfusion fluid is oxygenized and circulated by a gas lift. It is directed through the segment by two three-way taps. For safe and easy decontamination of radioactive substrates, the system is made entirely of glass. To perfuse fragile segments from small animals such as mice and rat pups in vitro, the perfusion pressure had to be reduced to 15 cm H2O column. Therefore, the design of the perfusator was changed, and the gas lift and the three-way taps were moved to the side. With segments from adult rats, the modified perfusor yielded the same transfer data for 59Fe, glucose, and water as did the standard device. Experiments with proximal and distal segments from mice and rat pups showed a longitudinal pattern of adaptation during maturation as well as due to iron deficiency that was in accordance with expectations extrapolated from literature.
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PMID:A modified device for the differentiated study of intestinal transfer in isolated intestinal segments from mice and suckling rats in vitro. 904 Jan 12


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