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

Dietary iron deficiency (ID) decreases iron-containing proteins and hence respiratory capacity of skeletal muscle mitochondria (SMM), but noniron components are much less affected. Using a hexokinase plus glucose ATP-utilizing system, we studied control of respiration in isolated SMM from rats of variable iron status: ID, ID 3 days after intraperitoneal treatment with iron dextran, and control. We found that sensitivity of respiratory control (e.g., ATP/ADP at a given oxygen consumption) was positively related to state 3 respiratory capacity. Titration studies with carboxyatractyloside, a noncompetitive inhibitor of adenine nucleotide translocase (AdNT), revealed that AdNT concentration was unaffected by iron status. However, the turnover number of AdNT was markedly reduced by ID and improved with iron treatment. We conclude that in ID SMM, decreased maximal respiratory capacity is paralleled by impaired sensitivity to putative controllers of oxidative phosphorylation at any respiratory rate, despite normal levels of AdNT. A second study was designed to determine possible consequences of impaired sensitivity of respiratory control on motor unit recruitment during exercise. ID and normal rats were subjected to a program of walking treadmill exercise. Although exercise failed to induce any changes in oxidative enzyme levels in control rat, ID animals and exhibited substantial mitochondrial enzyme adaptation in hindlimb skeletal muscle. Furthermore, the most consistent enzymatic changes were observed to occur in fast glycolytic muscle fibers. These results suggest marked alterations in the pattern of muscle fiber recruitment during mild exercise in ID rodents and support the hypothesis that sensitivity of respiratory control in SMM is an important determinant of motor unit recruitment during aerobic exercise.
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PMID:Impaired control of respiration in iron-deficient muscle mitochondria. 261 Feb 48

18 components of metabolism were determined in the red cells of iron-deficient patients and data were expressed per 10(12) red cells to avoid the complicating effects of hypochromia and microcytosis. Glucose consumption, AMP and ATP, glycolytic intermediates except 2,3-bisphosphoglycerate (2,3-DPG) and phosphoenolpyruvate (PEP), red-cell Na+ and the net passive leakage of Na+ and K+ at 4 degrees C were all normal. Creatine, 6-phospho-D-gluconate: NADP oxidoreductase (6PGD) activity and fresh red-cell K+ were raised, suggestive of a young cell population. However, ATP: D-fructose-6-phosphate 1-phosphotransferase (PFK) activity and ADP were low. An elevated 2,3-DPG level was attributable to the anaemia present but the somewhat raised PEP level is unexplained. It is concluded that red cells in iron deficiency show some characteristics of a young cell population; in other respects they appear normal, but in containing a low PFK activity they are abnormal.
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PMID:Red-cell metabolism in patients with iron deficiency. 294 51

Nutritional iron deficiency induced in rats causes a significant reduction in level of brain nonheme iron and is accompanied by selective reduction of dopamine D2 receptor Bmax. Our previous studies have clearly demonstrated that these alterations can be restored to normal by supplementation with ferrous sulfate; however, neither brain nonheme iron level nor dopamine D2 receptor Bmax can be increased beyond control values even after long-term iron therapy. The possibility that iron deficiency can induce the breakdown of the blood-brain barrier (BBB) was examined. A 70 and 100% increase in brain uptake index (BUI) for L-glucose and insulin, respectively, were noted in iron-deficient rats. However, the BUI for valine was decreased by 40%, and those for L-norepinephrine and glycine were unchanged. In addition, it was demonstrated that in normal rats insulin is transported into the brain. The data show that iron deficiency selectively affects the integrity of the BBB for insulin, glucose, and valine transport. Whether the effect of iron deficiency on the BBB is at the level of the capillary endothelial cell tight junction is not yet known. However, this study has shown that an important nutritional disorder (iron-deficiency anemia) has a profound effect on the BBB and brain function.
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PMID:Selective alteration in blood-brain barrier and insulin transport in iron-deficient rats. 296 35

Iron deficient (ID) and control (C) rats were studied to determine if severe iron deficiency alters insulin-stimulated glucose disposal. Euglycemic hyperinsulinemic glucose clamps were conducted by infusing insulin (2 m mu.kg-1.min-1, constant rate) for 120 min while maintaining euglycemia. In a 12-h fasted state, ID rats were hyperglycemic (109.4 +/- 4.0 mg.dL-1 arterial plasma glucose, x +/- SEM) when compared with C rats (86.9 +/- 3.4 mg.dL-1) (P less than 0.05). Even though insulin was infused identically on a per kilogram body weight basis for both groups, the resulting hyperinsulinemia was higher in ID rats (3.1 +/- 0.27 ng.mL-1) compared with C rats (2.3 +/- 0.4 ng.mL-1) at the end of the clamp. Glucose infusion rates required to maintain euglycemia were twofold higher in ID rats (27.0 +/- 5.4 mg.kg-1.min-1) versus C rats (13.1 +/- 3.3 mg.kg-1.min-1) (P less than 0.05). Circulating lactic acid increased in both groups, and the concentrations in ID rats (3.2 +/- 0.4 mmol.L-1) were significantly higher than those in C rats (1.8 +/- 0.5 mmol.L-1) at the end of the clamp. When the efficiency of insulin to dispose glucose was evaluated by calculating the glucose disposal divided by the prevailing insulinemia, ID rats could dispose of almost twice the glucose per unit of insulin [9.0 +/- 0.6 (mg.kg-1.min-1)/(ng.mL-1)] when compared with C rats [5.6 +/- 0.9 (mg.kg-1.min-1)/(ng.mL-1)] (P less than 0.05). The data indicate that insulin sensitivity is increased in ID rats and that ID rats cannot metabolize exogenous insulin as well as C rats.
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PMID:Increased insulin sensitivity in iron-deficient rats. 304 44

Copper is known to be an essential nutrient for human beings, but a Recommended Dietary Allowance has not yet been established. A safe and adequate range of intake was established in 1980 for copper and five other trace elements. The range for copper, 2 to 3 mg/day, is higher than the usual dietary copper intake of many individuals in this country. On the basis of balance studies, a requirement of 1.3 mg/day has been suggested. Recent data on copper intake and bioavailability should aid in reevaluating the dietary copper requirement. Copper deficiency symptoms have seldom been observed in human beings. When copper deficiency has been recognized, it has been under unusual conditions, such as in patients receiving parenteral nutrition. Interactions between copper and other dietary components may alter copper status, but the impact of those interactions is not yet well understood. Dietary factors that may affect the bioavailability of copper include the levels of copper, zinc, and molybdenum in the diet; iron deficiency; ascorbic acid intake; intake of carbohydrates, including fructose, glucose, and starch; and fiber and phytate intakes. Some drugs may also affect copper bioavailability.
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PMID:Copper nutriture, bioavailability, and the influence of dietary factors. 327 98

Rates of blood glucose and lactate turnover were assessed in resting iron-deficient and iron-sufficient (control) rats to test the hypothesis that dependence on glucose metabolism is increased in iron deficiency. Male Sprague-Dawley rats, 21 days old, were fed a diet containing either 6 mg iron/kg feed (iron-deficient group) or 50 mg iron/kg feed (iron-sufficient group) for 3-4 wk. The iron-deficient group became anemic, with hemoglobin levels of 6.4 +/- 0.2 compared with 13.8 +/- 0.3 g/dl for controls. Rats received a 90-min primed continuous infusion of D-[6-3H]glucose and sodium L-[U-14C]lactate via a jugular catheter. Serial samples were taken from a carotid catheter for concentration and specific activity determinations. Iron-deficient rats had significantly (P less than 0.05) higher blood glucose (7.1 +/- 0.3 vs. 6.1 +/- 0.2 mM) and lactate concentrations than controls (1.0 +/- 0.1 vs. 0.8 +/- 0.1 mM). The iron-deficient group had a significantly higher glucose turnover rate (67 +/- 2 vs. 58 +/- 4 mumol . kg-1 . min-1) than the control group. Significantly more metabolite recycling in iron-deficient rats was indicated by greater incorporation of 14C (from infused [14C]-lactate) into blood glucose. Assuming a carbon crossover correction factor of 2, half of blood glucose arose from lactate in deficient animals. By comparison, only 25% of glucose arose from lactate in controls. Lack of a difference in lactate turnover (irreversible disposal) rates between deficient rats and controls (191 +/- 26 vs. 163 +/- 15 mumol . kg-1 . min-1) was attributed to 14C recycling.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Increased glucose dependence in resting, iron-deficient rats. 366 3

Rhizobium leguminosarum GF160 required iron for growth under aerobic conditions in a chemically defined medium. Maximal growth of bacteria previously depleted in iron was obtained with approximately 50 microM unchelated ferric iron and with glucose as the only carbon source. Growth under iron deficiency did not result in the production of detectable levels of siderophores of either the catechol or hydroxamate types. Growing cells released a Fe3+-reducing agent that was identified as anthranilic acid by paper and thin-layer chromatography, ultraviolet and nuclear magnetic resonance spectroscopy, and mass spectrometry. The amount of anthranilic acid secreted per unit of cell growth was inversely related to the iron concentration in the culture medium and reached concentrations up to 1 mM. Ferric but not ferrous ions were solubilized in the growth medium by anthranilic acid.
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PMID:Iron requirement of Rhizobium leguminosarum and secretion of anthranilic acid during growth on an iron-deficient medium. 372 13

Eighty-five consecutive general hospital patients requiring total parenteral nutrition (TPN) were prospectively studied in order to evaluate the safety and efficacy of a '3-in-1' nutrient mixture. All formulas were individualized to estimated requirements (average composition nitrogen 14 g, glucose 350 g, fat 50 g), mixed in the hospital pharmacy, contained within 3-litre EVA plastic bags, and given to the patients as a continuous 24-hour infusion. The average duration of TPN was 19 days per patient (range 8 - 84 days). Judging by nitrogen balance and plasma protein concentrations, the system was effective in maintaining or improving nutritional status in patients in a relatively stable condition but not in those who were critically ill (e.g. those in an intensive care unit). Development of magnesium and iron deficiencies was common during the period of TPN (25% of patients developing magnesium deficiency and 40% developing iron deficiency) despite daily supplementation with commercial trace element mixtures, but these states were easily corrected by high-dose administration. 'Creaming' of less than 5 mm on the surface of the emulsion was common, whereas that of more than 10 mm was rare (12 bags) and invariably associated with excessive addition of polyvalent cation or glucose. Deposition of lipid on the internal surface of the catheter was a common problem after 2 weeks' continuous administration. Temporary problems with faulty bag connections resulted in excessive catheter sepsis (14%) due to Staphylococcus epidermidis. Mild reversible disturbances in liver function occurred in one-third of the patients. The system appears safe and effective for the management of most patients requiring long-term TPN.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical evaluation of a '3-in-1' intravenous nutrient solution. 392 69

To test the hypothesis that glucose metabolism is altered by iron deficiency, rates of glucose turnover and oxidation were assessed concurrently with the metabolic rate (VO2) in iron-deficient anemic rats and in normal rats at rest. Male Sprague-Dawley rats, 21 days old, were fed a diet containing either 6 mg iron/kg feed (iron-deficient group) or 50 mg iron/kg feed (iron-sufficient control group) for 3-4 wk. After dietary treatment the iron-deficient group was anemic, with hemoglobin levels of 5.8 +/- 0.2 g/dl, compared with 13.8 +/- 0.4 g/dl for controls. To study glucose metabolism, rats received a 90 min primed-continuous infusion of [6-3H]-and [U-14C]glucose via an indwelling jugular catheter. Serial blood samples were removed from a carotid catheter for determination of glucose concentration and specific activity. Expired air was monitored for VO2, VCO2, and 14CO2. The VO2 (ml X kg-1 X min-1) of iron-deficient rats was 20% higher than controls. Iron-deficient rats had a greater rate of glucose turnover (94 +/- 4 vs. 52 +/- 3 mumol X kg-1 X min-1) and a greater glucose recycling rate, even when normalized to VO2. Despite a higher blood glucose concentration (5.5 +/- 0.6 vs. 4.1 +/- 0.1 mM), the metabolic clearance rate was greater in iron-deficient animals (18 +/- 1 vs. 13 +/- 1 ml X kg-1 X min-1).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Glucose turnover and oxidation are increased in the iron-deficient anemic rat. 396 82

Growth of Bacillus stearothermophilus strain NCA 1518 Smooth in Dextrose Tryptone Agar (DTA) was inhibited by sodium caseinate. Binding studies indicated that sodium caseinate, when present in DTA, had the capacity to effect an iron deficiency which could cause inhibition of growth. Additions of essential cations, iron (1 mM), calcium (5 mM), magnesium (10 mM), or hydrogen ion (pH 5.7), relieved inhibition. Responses to and interactions among these relief factors were analyzed statistically. Equations were fitted to the data and were used to estimate responses to all treatment combinations within the ranges tested. Results from these studies indicated that calcium, magnesium, and hydrogen ion acted by decreasing the binding capacity of the protein for iron, rendering this metal available for metabolic needs. Evidence was obtained that ferrous rather than ferric iron was the limiting factor in DTA containing sodium caseinate.
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PMID:Relief of casein inhibition of Bacillus stearothermophilus by iron, calcium, and magnesium. 569 3


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