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

There is increasing evidence both from 'association' and 'intervention' studies that iron deficiency has an adverse effect on brain function in animals and children. The severity and duration of iron deficiency are important in determining the effect on development. Iron replacement therapy has immediate (within 14 days) and long-term (over 3 months) beneficial effects on behaviour and psychomotor development. The mechanisms for this probably involve a number of biochemical pathways in which iron is essential. These include mitochondrial enzymes and various neurotransmitters. Cytochrome C is reduced by iron deficiency but brain tissue is relatively spared until the deficiency is severe. Levels of neurotransmitters such as noradrenaline, serotonin and dopamine are all altered during iron deficiency and this may explain some of the behavioural and developmental changes that occur.
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PMID:Iron deficiency and the brain. 248 88

The reports that iron-deficiency anemia in human subjects induces behavioral changes was investigated in rats made nutritionally iron-deficient. The most prominent features of these animals were: the unchanged metabolism of the neurotransmitters noradrenaline, dopamine and serotonin, profound reduction of brain nonheme iron, the selective diminution of dopamine D2 receptor number (measured by Bmax), modification of dopamine-dependent behaviors and reduction of learning processes. The induction of these changes and their recovery with iron supplementation are age- and time-dependent phenomena. In newborn rats, however, the consequences of iron deficiency are irreversible, even after long-term iron supplementation. The results point to the profound effect iron metabolism can have on the long-term development and function of dopaminergic neurotransmission. These findings may not be totally unexpected, since iron distribution in the brain is highly localized in dopaminergic-peptidergic regions, such as the globus pallidus, substantia nigra, red nucleus, thalamus, caudate nucleus and nucleus accumbens. In some regions its concentration is higher than that found in the liver, the site of iron metabolism.
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PMID:Minimal brain damage induced by early iron deficiency: modified dopaminergic neurotransmission. 303 48

Norepinephrine turnover and energetic efficiency studies were conducted in three groups of male Sprague-Dawley rats placed on low iron diets for 5 weeks on weaning. Iron-deficient rats had significant anemia (hematocrit less than 20%) and growth retardation relative to pair-fed and ad libitum fed controls who received the same diet plus weekly iron dextran injections. Energetic efficiency over a 7-day period was nearly 30% less in anemic animals. This was associated with significantly higher rates of norepinephrine turnover in brown adipose tissue (110%) and heart (330%) with significant hypertrophy in both tissues. There was no difference in body composition in ad libitum groups. Plasma triiodothyronine and thyroxine were reduced by 37% in iron deficients compared to controls. Thus 39% increase in caloric requirements in iron deficiency is associated with increased sympathetic and perhaps thermogenic activity in brown adipocytes.
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PMID:Feed efficiency and norepinephrine turnover in iron deficiency. 382 10

The effect of sucrose overfeeding and low iron diet on brown adipose tissue (BAT) thermogenesis of rats has been investigated from the view point of in vitro BAT oxygen consumption and BAT fatty acids (FA) compositions in rats. Control group was fed on a standard diet with tap water, sucrose group was on the standard diet and 32% sucrose solution, and iron deficient group on a low iron diet with tap water. In vitro interscapular BAT thermogenesis as estimated by oxygen consumption was measured in minced tissue blocks in Krebs-Ringer phosphate buffer using a Clark oxygen electrode. In sucrose overfeeding rats, caloric intake was greater than in controls, but did not differ body weight. Interscapular BAT weight and DNA content were greater. Colonic and tail skin temperatures were higher. Basal oxygen consumption was higher. Noradrenaline- and glucagon-stimulated oxygen consumptions did not differ when expressed per DNA, but significantly greater per whole tissue pad. Both BAT-triglyceride (TG) and -phospholipid (PL) levels were higher. Polyunsaturated FA were lower, while monosaturated FA were higher in both BAT-TG and -PL. In iron deficient rats, BAT weight and DNA content were higher. Colonic and tail skin temperatures did not differ. Although basal oxygen consumption did not differ, noradrenaline-stimulated oxygen consumption was less per DNA, but did not differ per whole tissue pad, while glucagon-stimulated oxygen consumption was less when expressed per DNA, as well as whole tissue pad. Cold-tolerance as assessed by the fall in colonic temperature at 0 degree C was decreased. BAT-TG and -PL levels did not differ. Polyunsaturated FA were higher in both BAT-TG and -PL. These findings indicated that sucrose-induced overfeeding enhances BAT thermogenesis mainly by tissue hyperplasia, while iron deficiency suppresses BAT thermogenic response, although it causes the compensatory tissue hyperplasia.
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PMID:[Nutritional adaptation in brown adipose tissue thermogenesis--with special reference to overfeeding and iron deficiency]. 786 52

Iron homeostasis is essential for the integrity of brain monoaminergic functions and its deregulation might be involved in neurological movement disorders such as the restless legs syndrome (RLS). Although iron metabolism breakdown concomitantly appears with monoaminergic system dysfunction in iron-deficient rodents and in RLS patients, the direct consequences of peripheral iron deficiency in the central nervous system (CNS) of non-human primates have received little attention. Here, we evaluated the peripheral iron-depletion impact on brain monoamine levels in macaque monkeys. After documenting circadian variations of iron and iron-related proteins (hemoglobin, ferritin and transferrin) in both serum and cerebrospinal fluid (CSF) of normal macaques, repeated blood withdrawals (RBW) were used to reduce peripheral iron-related parameter levels. Decreased serum iron levels were paradoxically associated with increased CSF iron concentrations. Despite limited consequences on tissue monoamine contents (dopamine - DA, 3, 4-dihydroxyphenylacetic acid - DOPAC, homovanillic acid, L-3, 4-dihydroxyphenylalanine - L-DOPA, 5-8 hydroxytryptamine - 5-HT, 5-hydroxyindoleacetic acid - 5-HIAA and noradrenaline) measured with post-mortem chromatography, we found distinct and region-dependent relationships of these tissue concentrations with CSF iron and/or serum iron and/or blood hemoglobin. Additionally, striatal extracellular DA, DOPAC and 5-HIAA levels evaluated by in vivo microdialysis showed a substantial increase, suggesting an overall increase in both DA and 5-HT tones. Finally, a trending increase in general locomotor activity, measured by actimetry, was observed in the most serum iron-depleted macaques. Taken together, our data are compatible with an increase in nigrostriatal DAergic function in the event of iron deficiency and point to a specific alteration of the 5-HT/DA interaction in the CNS that is possibly involved in the etiology of RLS.
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PMID:Blood withdrawal affects iron store dynamics in primates with consequences on monoaminergic system function. 2566 8