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

The interactive effect of iron deficiency and dietary carbohydrate type on growth and thyroid hormone status of Sprague-Dawley rats was studied. Rats were fed either an iron-adequate (approximately 35 micrograms Fe/g) or an iron-deficient (less than 3 micrograms Fe/g) diet that contained 70% carbohydrate. The carbohydrate sources were 100% cornstarch (STARCH), 85.7% cornstarch and 14.3% sucrose (STARCH/SUCR), 71.4% cornstarch, 14.3% sucrose and 14.3% dextrin (DEXTRIN), or 100% sucrose (SUCROSE). After 4 wk, iron-deficient rats weighed less than the iron-adequate rats and were severely anemic. Total food intake was lower in iron-deficient than in iron-adequate animals; it was also significantly lower in SUCROSE-fed animals relative to other carbohydrate groups. Plasma glucose concentrations were significantly higher in iron-deficient rats than in iron-adequate rats, but plasma thyroid hormones, thyroxine and triiodothyronine, and liver thyroxine monodeiodinase activity were lower. Deiodination of reverse triiodothyronine in liver was unaffected by iron deficiency regardless of carbohydrate treatment. The STARCH-fed animals had higher rates of hepatic thyroxine monodeiodinase activity than rats fed the other dietary carbohydrates. The two main conclusions from this study are that thyroid hormone metabolism is altered by iron deficiency regardless of food intake and that the best purified rodent diet for this type of study would contain a mixture of carbohydrate types to avoid the stimulation of thyroxine monodeiodinase by a 70% cornstarch diet.
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PMID:Type of dietary carbohydrate affects thyroid hormone deiodination in iron-deficient rats. 156 71

Iron-deficient anemic rats have previously been shown to have low plasma levels of thyroid hormone and a poor plasma thyroid hormone response to acute cold exposure. As an initial exploration, we examined thyroid hormone metabolism during iron deficiency in age-matched rats from three aspects: 1) plasma TSH (thyrotropin, thyroid stimulating hormone), T4 (thyroxine) and T3 (triiodothyronine) responses to graded doses of exogenous TRH (thyrotropin releasing hormone), 2) plasma T3 kinetics, and 3) rates of hepatic T3 production. Iron-deficient anemic rats had lower basal TSH values and blunted TSH responses to intravenous TRH injection at three different doses (10, 25 and 50 ng TRH/100 g body wt). Iron-deficient anemic rats also had a significant decrease in plasma T3 turnover (42 vs. 88 ng/h in controls), and significantly lower hepatic T4-5'-deiodinase activities than controls [26 vs. 44.0 ng T3/(mg protein.20 min)]. Thus, decreased rates of T3 production in iron-deficient anemic rats, as documented by turnover studies, may be related to decreased deiodinase activity and reduced peripheral formation of T3. The dampened TSH responses to TRH further facilitate or perpetuate this T3 deficiency. We propose that this abnormal thyroid state is partially responsible for impaired thermogenesis in iron-deficiency anemia.
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PMID:Evidence for thyroid hormone deficiency in iron-deficient anemic rats. 249 73

The effects of two dietary treatments on norepinephrine turnover in iron deficiency were examined. These studies were designed to bridge the gap between previous studies of poor thermoregulation in iron deficiency which used a diet (HMW, Hubbel-Mendel-Wakeman formulation) relatively high in fat (46% of calories) and moderate in carbohydrate (46% of calories) and the more recent studies of thermogenesis in iron deficiency which use the AIN-76 recommended diet which is relatively low in fat (11% of calories) and high in carbohydrate (67% of calories). Iron deficient rats grew less well and had depressed thyroid hormone concentrations regardless of dietary treatment group. The HMW diet significantly increased norepinephrine turnover in heart in iron deficient animals relative to AIN diet but had no effect in controls. Brown adipose tissue norepinephrine turnover was threefold higher in HMW rats fed a low iron diet, and only 67 percent higher in control rats. This study demonstrates that certain modest macronutrient manipulations affect norepinephrine content and turnover more in iron deficient than controls. However, abnormalities in thyroid hormone concentrations persist in iron deficient animals regardless of these dietary treatments.
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PMID:Norepinephrine turnover in iron deficiency: effect of two semi-purified diets. 276 48

When exposed to an ambient temperature of 4 degrees C, iron-deficient anemic rats become hypothermic. This lesion is related more to anemia than to tissue iron deficiency, since exchange transfusion to hematocrits over 25 restored normal thermoregulatory performance. Likewise poor cold responses were induced in control rats by transfusion to low hematocrits. Cold sensitivity in all anemic animals was paralleled by poor thyroid responses: there was a significant positive correlation between hematocrit and percent rise in triiodothyronine (r = 0.63) and thyroxine (r = 0.53) during 6 h at 4 degrees C. Basal levels of thyroid-stimulating hormone (TSH) were similar in control and iron-deficient animals: after cold exposure, TSH rose to higher levels in those animals with hematocrits over 25 than in those with lower hematocrits. Diminished O2 delivery to tissues responsible for heat production is probably a major component of the cold sensitivity of anemic rats. The novel finding that thyroid hormone responses are compromised by anemia implies effects on hormonal regulation that may also contribute to this functional lesion.
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PMID:Effect of iron-deficiency anemia on hormone levels and thermoregulation during cold exposure. 674 20

To determine if the previously observed alterations in norepinephrine (NE) metabolism and resting metabolic rate in iron-deficient (ID) rats result from hypothyroidism, exogenous thyroxine (T4) and 3,5,3'-triiodothyronine (T3) were administered to ID rats in doses sufficient to normalize the plasma concentrations of these hormones, whereas other ID and control (CN) rats received placebo treatment. Resting oxygen consumption was approximately 25% higher in ID than CN rats; T4 but not T3 treatment alleviated this elevated oxygen uptake. The NE content of interscapular brown adipose tissue (IBAT), liver, and heart was 70-80% lower in ID than CN rats, and NE turnover in the same tissues was likewise 40-60% lower in ID than CN rats, with no systematic effect of either T3 or T4 treatment. Liver T(4)5'-deiodinase activity was 70% lower in ID than CN rats and increased with T4 but not T3 treatment. These experiments show that iron deficiency alters NE and energy metabolism in a way that is mostly independent of its effects on thyroid hormone metabolism.
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PMID:Effect of thyroid hormone replacement in iron-deficient rats. 750 3

The effects of different dietary fats on thyroid indices were studied in weanling iron-deficient rats. Rats were fed one of five different diets (safflower oil with a casein protein source, safflower oil with defatted beef as the protein source, prime rib, beef tallow with casein and stearate with casein). Both dietary fat and iron status (adequate, CN; deficient, ID; or iron-deficient replete, ID-replete) had significant effects on body weight and hemoglobin concentrations. The tallow-fed animals weighed the least relative to animals fed the other fats; ID rats were smaller than CN rats. The tallow- and stearate-fed animals had the highest hemoglobin concentrations. Type of dietary fat affected plasma thyroxine (T4), but not plasma triiodothyronine (T3) or rate of deiodination of reverse T3 (rT3). Iron deficiency decreased plasma concentrations of T3 and T4 and increased in vitro hepatic rT3 deiodination, suggesting that the ID animals tend to metabolize thyroid hormones via deactivating pathways. The alterations in thyroid hormone metabolism associated with iron deficiency are reversible with iron repletion.
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PMID:In vitro hepatic thyroid hormone deiodination in iron-deficient rats: effect of dietary fat. 835 Jun 75

Iron deficiency anemia is associated with lower plasma thyroid hormone concentrations in rodents and, in some studies, in humans. The objective of this project was to determine if plasma triiodothyronine (T3) and thyroxine (T4) kinetics were affected by iron deficiency. Studies were done at a near-thermoneutral temperature (30 degrees C), and a cool environmental temperature (15 degrees C), to determine plasma T3 and T4 kinetics as a function of dietary iron intake and environmental need for the hormones. Weanling male Sprague-Dawley rats were fed either a low Fe diet [iron-deficient group (ID), <5 microg/g Fe] or a control diet [control group (CN), 35 microg/g Fe] at each temperature for 7 wk before the tracer kinetic studies. An additional ID group receiving exogenous thyroid hormone replacement was also used at the cooler temperature. For T4, the disposal rate was >60% lower (89 +/- 6 vs. 256 +/- 53 pmol/h, P < 0.001) in ID rats than in controls at 30 degrees C, and approximately 40% lower (192 +/- 27 vs. 372 +/- 26 pmol/h, P < 0.01) in ID rats at 15 degrees C. Exogenous T4 replacement in a cohort of ID rats at 15 degrees C normalized the T4 concentration and the disposal rate. For T3, the disposal rate was significantly lower in ID rats in a cool environment (92 +/- 11 vs. 129 +/- 11 pmol/h, P < 0.01); thyroxine replacement again normalized the T3 disposal rate (126 +/- 12 pmol/h). Neither liver nor brown fat thyroxine 5'-deiodinase activities were sufficiently different to explain the lower T3 disposal rates in iron deficiency. Thus, plasma thyroid hormone kinetics in iron deficiency anemia are corrected by simply providing more thyroxine. This suggests a central regulatory defect as the primary lesion and not peripheral alterations.
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PMID:Plasma thyroid hormone kinetics are altered in iron-deficient rats. 968 62

Table salt can now be fortified with iodine and iron without interaction and without loss of potency. According to Levente Diosady, professor of Food Engineering at the University of Toronto, the amounts of the two micronutrients available to the human body have been significantly reduced when the two interacted. In the new technology, the iodine is covered with a dextrin (a water soluble starch) capsule that serves as a physical barrier to the iron. Micronutrient Initiative (an international secretariat based at IDRC that works to eliminate health problems resulting from iron, iodine, and vitamin A deficiencies) and IDRC supported the development of the technology. The efficiency of absorption of the two micronutrients in the new double fortified salt in the human body is being tested at the Hospital for Sick Children in Toronto. Later testing will be conducted by University of Ghana scientists in IDRC-funded trials that will focus on women and their families in areas of Ghana where these deficiencies are endemic. Iodine is part of thyroid hormone, which contributes to brain development in the fetus and regulates human metabolism; iodine deficiency is the most frequent cause of preventable mental retardation. Related disorders include lethargy, physical disabilities, goiter, stillbirth, and neonatal death. Iron deficiency, the most common nutritional problem in the world (particularly among women, infants, and children), is associated with anemia, fatigue, learning problems, pregnancy complications, premature births, and maternal mortality. The two deficiencies together affect more than one-third of the world's population. Approximately 1.6 billion people, in more than 100 countries, live in areas where iodine is not available in sufficient amounts; those most at risk include about one-third of China's population. It is also a severe problem in the Himalayas, the Andes, India, and West Africa.
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PMID:Micronutrient deficiencies. Reports from the field -- Africa. 1229 Mar 27

Several minerals and trace elements are essential for normal thyroid hormone metabolism, e.g., iodine, iron, selenium, and zinc. Coexisting deficiencies of these elements can impair thyroid function. Iron deficiency impairs thyroid hormone synthesis by reducing activity of heme-dependent thyroid peroxidase. Iron-deficiency anemia blunts and iron supplementation improves the efficacy of iodine supplementation. Combined selenium and iodine deficiency leads to myxedematous cretinism. The normal thyroid gland retains high selenium concentrations even under conditions of inadequate selenium supply and expresses many of the known selenocysteine-containing proteins. Among these selenoproteins are the glutathione peroxidase, deiodinase, and thioredoxine reductase families of enzymes. Adequate selenium nutrition supports efficient thyroid hormone synthesis and metabolism and protects the thyroid gland from damage by excessive iodide exposure. In regions of combined severe iodine and selenium deficiency, normalization of iodine supply is mandatory before initiation of selenium supplementation in order to prevent hypothyroidism. Selenium deficiency and disturbed thyroid hormone economy may develop under conditions of special dietary regimens such as long-term total parenteral nutrition, phenylketonuria diet, cystic fibrosis, or may be the result of imbalanced nutrition in children, elderly people, or sick patients.
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PMID:The impact of iron and selenium deficiencies on iodine and thyroid metabolism: biochemistry and relevance to public health. 1248 69

Extensive data from animal and human studies indicate that iron deficiency impairs thyroid metabolism. The aim of this study was to determine thyroid hormone status in iron-deficient adolescent girls. By stepwise random sampling from among all public high schools for girls in Lar and its vicinity in southern Iran, 103 out of 431 iron deficient subjects were selected. Urine and serum samples were collected and assayed for urinary iodine and serum ferritin, iron, total iron binding capacity (TIBC), thyroid stimulating hormone (TSH), thyroxine (T4), triiodothyronine (T3), free thyroid hormones (fT4 and fT3), triiodothyronine resin uptake (T3RU), reverse triiodothyronine (rT3), selenium and albumin concentrations. Hematological indices for iron status confirmed that all subjects were iron-deficient. There was a significant correlation between T4 and ferritin (r = 0.52, P < 0.001) and between TSH and ferritin (r = -0.3, P < 0.05). Subjects with low serum ferritin had a higher ratio of T3/T4 (r = -0.42, P < 0.01). Using stepwise regression analysis, only ferritin contributed significantly to the rT3 concentration (r = -0.35, P < 0.01). The results indicate that the degree of iron deficiency may affect thyroid hormone status in iron-deficient adolescent girls.
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PMID:The relationship between iron status and thyroid hormone concentration in iron-deficient adolescent Iranian girls. 1650 Aug 78


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