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

Young chicks were fed diets deficient in proteins, iron, niacin or thiamin to study the effects on various parameters of mineral metabolism in the duodenal mucosa. None of the treatments affected mucosal alkaline phosphatase activity; however, a five-day deprivation of protein reduced the inorganic phosphate content of mucosal cell nuclei. Iron deficiency reduced mucosal Ca, Zn, Fe and phosphate content, while niacin deficiency decreased mucosal Ca and phosphate. Thiamin deficiency reduced only the phosphate centent of intestinal mucosa. Duodenal phosphatase activity was positively correlated with tissue Ca and Fe and negatively with Zn.
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PMID:Relationship of dietary protein, iron, niacin or thiamin to intestinal mineral metabolism. 60 17

The effect of 10 days of total fasting (energy deprivation) on blood polymorphonuclear granulocyte functions, leukocyte numbers, iron and transferrin levels was evaluated in 14 healthy, normal-weight males. Granulocytes from 7 of the subjects were tested in vitro. A statistically significant depression was noted in their bactericidal capacity against Staph. aureus. The 14 subjects showed a marked decrease in the stainable activity of granulocyte alkaline phosphatase and decreases were noted in plasma iron and serum transferrin levels. The iron saturation of serum transferrin was unchanged. Thus, impairment of granulocyte bactericidal functions may occur secondarily to short-term total energy deprivation, in the absence of iron deficiency.
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PMID:Fasting (acute energy deprivation) in man: effect on polymorphonuclear granulocyte functions, plasma iron and serum transferrin. 96 52

Dietary intake and biochemical nutritional status was studied in patients who had undergone total gastrectomy (TG, n = 10) or partial gastrectomy (PG, n = 10) several years ago. The dietary intake of energy, macronutrients and micronutrients was very similar in the two groups and was also similar to the intake reported for healthy subjects in Sweden. The concentration of alpha-tocopherol in serum was subnormal in the TG group and that of carotene in both groups of patients, and the values were also significantly lower in the TG group than in the PG group. This was probably due to fat malabsorption, since dietary intake was found to be adequate. The proportions of n-6 and n-3 polyunsaturated fatty acids in serum phosphatidylcholine were not significantly different between the TG and PG groups. Iron deficiency was found in three patients in the TG group. Three patients (two TG, one PG) had elevated serum alkaline phosphatase and one patient (PG) had subnormal cobalamin concentration. For ascorbic acid, folate, calcium, phosphorus, magnesium, zinc, copper and selenium, the serum concentrations were normal or close to normal. Although the stores of some micronutrients seemed smaller after total gastrectomy, no major differences in nutritional status were found between the TG and PG groups. For the demonstration of decreased micronutrient stores during long-term follow-up after gastrectomy, an extended profile of biochemical markers of nutritional status is recommended.
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PMID:Nutrient intake and biochemical markers of nutritional status during long-term follow-up after total and partial gastrectomy. 160 Sep 23

Previous studies have documented decreased activities of certain enzymes and altered function in polymorphonuclear leukocytes (PMN) during iron deficiency. The present study was undertaken to determine if the enzymatic abnormalities could be correlated with morphologic or quantitative change in PMN granules. Ultrastructural examination of primary and secondary granules and assessment of the secondary granule components alkaline phosphatase and vicinal glycol-containing glycoconjugates was performed in rabbit bone marrow, peripheral blood, and peritoneal heterophils. In addition, biochemical quantifications of the secondary granule component alkaline phosphatase and the primary granule marker beta-glucuronidase were performed. The results confirmed that a marked, significant decrease in alkaline phosphatase occurs in iron-deficient animals; however, no biochemical decrease in beta-glucuronidase activity was observed. Ultrastructurally, PMN secondary granules of iron-deficient rabbits tended to be more numerous than in controls when examined with morphometric and glycoconjugate staining methods, but lacked staining in alkaline phosphatase preparations. These results demonstrate that iron-deficient rabbits produce normal to increased quantities of primary and secondary granules, despite a uniform deficiency of alkaline phosphatase, a secondary granule marker.
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PMID:Ultrastructural morphology and cytochemistry of iron-deficient polymorphonuclear leukocytes. 394 78

Twenty-six adult patients with histologically confirmed celiac disease on gluten-free diet after apparent disease remission were reexamined at 4-6 months intervals for a mean period of 55.4 months (range 13-137). Eight patients remained clinically well with normal blood tests. Eighteen patients had clinical or biological abnormalities. Eleven patients reported repeated episodes of meteorism and abdominal pain and/or diarrhea which disappeared in 2 after lactose withdrawal. Iron deficiency and macrocytic anemia were sometimes observed in 5 and 4 patients respectively. Altered plasma calcium, phosphorus and alkaline phosphatase and/or bone densitometry findings were detected in 7 patients. Seventeen patients (12 presenting some of the above findings) agreed to a repeat biopsy: 13 of these showed grade II and 4 grade III abnormalities. Although adult celiac patients may show marked improvement during gluten-free diet, minor clinical disturbances and biochemical abnormalities may still be present.
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PMID:Clinical, biochemical and histological abnormalities in adult celiac patients on gluten-free diet. 408 41

The effect of the iron-deficient diets on osseous tissue formation was studied in long-term experiments. During intense growth, iron deficiency led to a decrease in the content of hexosamines, in the activity of phosphomonoesterase I and calcium, delay in collagen maturation in the femoral bones, as well as to phosphorus-calcium metabolic disorders. Histological examination revealed thickening of the articular cartilage, an increase in the number and volume of osteocytes, islets of the proliferative osteocytes on the part of the endosteum, and a number of dystrophic abnormalities.
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PMID:[Effect of iron-deficient diets on the formation of bone tissue]. 651 86

Duodenal mucosa showed normal morphology, interepithelial lymphocytes, alkaline phosphatase, and sucrase in a girl with growth retardation and iron deficiency, but normal absorption of lactose and xylose after two years of abnormal stools. Mucosal lactase was low. Fourteen months later mucosal damage consistent with coeliac disease was evident, and gluten intolerance was subsequently confirmed by gluten challenge. It is probable that, in some children, the mucosal lesion occurs very gradually, so that at an early stage with normal morphology, suppression of lactase activity and possibly interference with iron absorption may be the only abnormalities.
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PMID:Early or pre-coeliac mucosa: development of gluten enteropathy. 746 78

Although body iron status modulates whole body retention of heme derived iron, it is not known with certainty whether modulation occurs by regulation of mucosal uptake of heme. In vivo uptake from perfused intestine of heme labeled with 14C in the porphyrin ring was studied in groups of rats of differing iron status ranging from fully replete to markedly iron deficient. Heme extraction from infusate and mucosal heme uptake were significantly different between test groups (P < 0.005 and 0.001, respectively). Marked iron deficiency induced a 4.8-fold rise in heme extraction relative to iron-replete animals; rats with latent iron deficiency showed a smaller but still significant rise. Heme extraction correlated negatively with indicators of iron status: hemoglobin (r = -0.76, P < 0.001) and serum iron (r = -0.56, P < 0.05). The specific binding of [14C]heme to purified brush borders from iron-replete and iron-deficient rats was 1.4-fold higher in deficient rats when expressed per milligram of protein (P = 0.046) and 3.3-fold higher when expressed relative to alkaline phosphatase activity (P = 0.014). Thus mucosal uptake of heme in iron deficiency is increased because of an increase in its binding to the brush border.
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PMID:Modulation of uptake of heme by rat small intestinal mucosa in iron deficiency. 823 54

Severe iron deficiency results in complex systemic disorders e.g., including metabolism of energy and minerals. To investigate whether also moderate iron depletion may alter the activities of citric cycle enzymes and the cytochrome oxidase, the trace element status, and serum enzymes indicative of cell damage, this experiment was carried out with rats supplied with sub-optimal iron (9, 13 and 18 mg iron per kg diet) over a total of 5 weeks. The study included 3 pair-fed groups and an ad libitum group, fed with 50 mg iron/kg diet. All iron-restricted rats were classified as iron-deficient on the basis of reduced iron concentrations in body and iron-depending blood parameters. Body weight gain and catalase activity in kidney were lowered in rats receiving the lowest dietary iron level, exclusively. Rats fed 9 and 13 mg iron per kg diet had nearly 6- and 3-fold, respectively higher platelet counts in blood than their corresponding pair-fed controls. The activities of transaminases ASAT and ALAT, alkaline phosphatase, glutamate dehydrogenase and lactate dehydrogenase in serum which are indicative of cell damage were also markedly influenced by moderate dietary iron restriction, in which the enzyme levels in serum increased with intensifying iron depletion. Although, moderate iron restriction to young male rats was associated with marked alterations in iron status and serum enzymes, the activities of tricarboxylic acid cycle enzymes including malic dehydrogenase, fumarase, and isocitric dehydrogenase as well as cytochrome oxidase in liver remained largely unaffected. Only hepatic aconitase showed a somewhat reduction with iron depletion. Moreover, iron restriction was also accompanied with an accumulation of copper in liver which was significant for rats fed 9 and 13 mg iron per kg diet, whereas zinc status remained completely unaffected by moderate iron deficiency. It can be concluded, that a short-term moderate iron deficiency with ranging hemoglobin concentrations from 66 and 121 g/L, was accompanied with altered platelet counts, serum enzyme activities indicative of cell damage, and hepatic copper concentrations, but the activities of the tricarboxylic acid cycle enzymes and cytochrome oxidase in liver remained largely unaffected.
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PMID:Effect of different degrees of moderate iron deficiency on the activities of tricarboxylic acid cycle enzymes, and the cytochrome oxidase, and the iron, copper, and zinc concentrations in rat tissues. 980 Mar 17

Redox-active forms of iron are known to catalyze free radical mediated peroxidative reactions. There is scanty information on such effects at the sites of iron absorption. This was tested in iron-deficient WKY female rats supplemented for 15 days with FeSO4 equivalent to 8 mg of iron (D+) and compared with iron deficient (D) and iron adequate (C) rats. The levels of intestinal MDA and protein carbonyls and the activities of various antioxidant enzymes were estimated. As markers of functional integrity, the activities of alkaline phosphatase and Lys-Ala-dipeptidyl aminopeptidase were evaluated. In addition, we measured the concentrations of ferritin, transferrin, and ceruloplasmin levels in serum and in intestinal mucosa. It was observed that correction of iron deficiency resulted in significant increase in MDA and protein carbonyl formation. Activities of both alkaline phosphatase and Lys-Ala-dipeptidyl aminopeptidase were significantly decreased in D+ compared to C. The increase in catalase and decrease in Gpx was found to be sensitive to iron administration. Neither iron deficiency nor its correction had any effect on the activity of SOD and GSH levels. Iron supplementation has resulted in decreased mobilization of stored iron as reflected by increased mucosal ferritin level and decreased serum ceruloplasmin ferroxidase activity contributing to greater peroxidative stress in the intestine. These results suggest that iron-deficient intestine of rat is more susceptible to iron-mediated peroxidative damage and functional impairment during correction of deficiency with iron.
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PMID:Iron-deficient intestine is more susceptible to peroxidative damage during iron supplementation in rats. 980 Oct 65


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