Gene/Protein Disease Symptom Drug Enzyme Compound
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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

For many decades there has been adequate information for the elimination of acute dietary deficiency diseases. Scurvy, beri-beri, and pellagra, once serious scourges, are now seen only rarely. The severe forms of protein-energy malnutrition, kwashiorkor and marasmus, have also decreased greatly. Nonetheless, mild to moderate forms of protein-energy deficiency, exacerbated by infection, continue to impair growth and development in a majority of the low-income pre-school age populations of most developing countries. Deficiencies of iron, iodine, and vitamin A are still widespread in developing countries. Fortunately, the success of the WHO/UNICEF "Child Survival and Development Revolution" in persuading most developing countries to introduce expanded programs of immunization, growth monitoring, and appropriate feeding of young children, control of diarrheal disease, and specific campaigns against avitaminosis A, iodine deficiency disorders, and the functional consequences of iron deficiency, will accelerate the decline of acute deficiency diseases in the developing world. Diets are changing among the more affluent in these countries, however, and it is time for them to stress dietary goals for the health of rich and poor alike. For the first time there is enough information regarding dietary risk factors for chronic disease to provide an opportunity in the 1990s to accelerate the dietary changes that have already brought significant health benefits to some populations in North America and Europe. The changes, which include a lower dietary intake of fat, particularly saturated fat, less salt, and more green and yellow vegetable and whole grain cereals, can be expected to influence favorably morbidity from cardiovascular diseases and some kinds of cancer. For maximum benefit, these measures need to be combined with the avoidance of obesity, reasonable physical activity, abstention from, or moderate use of, alcohol, and avoidance of tobacco in any form. Since there is already considerable momentum toward these changes in North America and some European countries, the 1990s are likely to see substantial further progress in the reduction of chronic diseases known to be influenced by diet.
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PMID:Nutrition: prospects for the 1990s. 219 71

A niacin-deficient purified amino acid diet that contained adequate (40 mg/kg) or deficient (10 or 15 mg/kg) iron was used to assess the growth promoting efficacy of tryptophan as a niacin precursor. Basal diets contained 1400 mg/kg tryptophan, a level that was established as meeting the requirement for tryptophan per se in diets containing excess nicotinic acid. Chicks fed the iron-deficient diets had markedly lower hemoglobin concentrations than those fed the iron-adequate diets. Regardless of iron level, chicks exhibited linear growth responses to either nicotinic acid or tryptophan supplementation. Using multiple-linear regression of weight gain on supplemental tryptophan or nicotinic acid intake, the efficiency (wt:wt) of tryptophan conversion to niacin activity (i.e., tryptophan slope divided by nicotinic acid slope) was a mean of 1.77% (56:1) for chicks fed the iron-deficient diet. This was significantly (P < 0.05) lower than the 2.39% (42:1) efficiency calculated for chicks fed the iron-adequate diet. Thus, iron deficiency reduced tryptophan utilization (for NAD synthesis) but had no effect on nicotinic acid utilization. The results suggest that pellagra in populations having endemic anemia and protein-energy malnutrition may be due not only to inadequate intakes of bioavailable niacin but also to inadequate intakes of bioavailable iron.
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PMID:Iron deficiency reduces the efficacy of tryptophan as a niacin precursor. 812 Jun 64

A child responds to a deficiency of an essential nutrient either by continuing to grow and consuming body stores with eventual reduction in the bodily functions (Type I) or by reducing growth and avidly conserving the nutrient to maintain the concentration of the nutrient in the tissues (Type II). Examples of Type I nutrient deficiency are anemia (iron deficiency), beri-beri (thiamin deficiency), pellagra (niacin or nicotinic acid deficiency), scurvy (vitamin C or ascorbic acid deficiency), xerophthalmia (vitamin A or retinol deficiency) and iodine deficiency disorders. Diagnosis is relatively simple via clinical symptoms and measurement of the concentration of the nutrient itself. There are no characteristic symptoms to distinguish which Type II nutrient deficiency an individual has; all deficiencies result in the poor growth, stunting, and wasting generally ascribed to protein-energy malnutrition. In Type II, growth stops, the body starts to conserve the nutrient, and its excretion falls to very low levels. In severe deficiency the body may start to break down its own tissues and the reduction of appetite accompanies this condition. An animal can die from zinc deficiency even though it is has a normal concentration of zinc in its tissues, but it can respond rapidly to small amount of dietary zinc. The mechanisms by which the body stops growing in response to nutritional lack are similar to the hormonal picture seen in endocrine disease (reduction of the production of the hormonal mediators of growth, down-regulation of receptors, and reduction of protein synthesis). Growth failure is the clinical sign characteristic of a diet deficient in protein, zinc, magnesium, phosphorus, and potassium. Wasting may be also ascribed to toxins, infection, worms, or persistent diarrhea. Anorexia is another common response in nutrient deficiency. Only a supplementation diet with a balance of nutrients will promote rapid recovery.
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PMID:Specific deficiencies versus growth failure: type I and type II nutrients. 1234 13