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Deficiency in humans

Magnesium ion is essential for normal Ca " and K" metaboHsm. In acute experimental magnesium deficiency in humans, hypocalcemia occurs despite adequate calcium intake and absorption and despite normal renal and parathyroid functions. Negative K" balance is also observed. AH biochemical and clinical abnormaHties disappear upon restoration of adequate amounts of magnesium to the diet (64). [Pg.381]

Pure selenium deficiency, without concurrent vitamin E deficiency, is not generally seen except in animals on experimental diets (113). In China, selenium deficiency in humans has been associated with Keshan disease, a cardiomyopathy seen in children and in women of child-bearing ages, and Kashin-Beck disease, an endemic osteoarthritis in adolescents (113). [Pg.386]

Deficiency or Toxicity in Humans. Molybdenum deficiency in humans results in deranged metaboHsm of sulfur and purines and symptoms of mental disturbances (130). Toxic levels produce elevated uric acid in blood, gout, anemia, and growth depression. Faulty utiH2ation results in sulfite oxidase deficiency, a lethal inborn error. [Pg.387]

An en2ymatic method for assessing riboflavin deficiency in humans has been developed (74). It is based on the fact that NADPH-dependent glutathione reductase of red cells reflects riboflavin fluctuations. [Pg.79]

The recommended daily allowance for vitamin E ranges from 10 international units (1 lU = 1 mg all-rac-prevent vitamin E deficiency in humans. High levels enhance immune responses in both animals and humans. Requirements for animals vary from 3 USP units /kg diet for hamsters to 70 lU /kg diet for cats (13). The complete metaboHsm of vitamin E in animals or humans is not known. The primary excreted breakdown products of a-tocopherol in the body are gluconurides of tocopheronic acid (27) (Eig. 6). These are derived from the primary metaboUte a-tocopheryl quinone (9) (see Eig. 2) (44,45). [Pg.147]

Symptoms of Essential Fatty Acid Deficiency in Humans Include Skin Lesions Impairment of Lipid Transport... [Pg.194]

Nishino S, Ripley B, Overeem S, et al. Hypocretin (orexin) deficiency in human narcolepsy. Lancet 2000 355 39-40. [Pg.632]

Selenium deficiency in humans occurs in the loessial region of the North China and Tibet Plateau of China (Liu, 1996). The arid and semi-arid soils in these areas of China contain low total Se in their parent materials. [Pg.263]

Copper deficiency in humans and other mammals is characterized by slow growth, hair loss, anemia, weight loss, emaciation, edema, altered ratios of dietary copper to molybdenum and other metals, impaired immune response, decreased cytochrome oxidase activity, central nervous system histopathology, decreased phospholipid synthesis, fetal absorption, and eventually death (NAS 1977 Gallagher 1979 Kirchgessner et al. 1979 USEPA 1980 ATSDR 1990 Percival 1995). [Pg.173]

Epileptiform fits associated with degenerative changes in the myelin sheath of peripheral nerves and spinal cord occur in B6-deficient animals. Lesions in the arteries, resembling those of human atherosclerosis, have been observed in Be-deficient monkeys. Recently, a state of Be deficiency in human infants, characterized by loss of ability to convert tryptophan to nicotinic acid, by impaired growth, convulsions, and hypochromic anemia, has been described, following omission of vitamin B6 from the diet. [Pg.212]

B36. Broquist, H. P., and Luhby, A. L., Detection and isolation of formimino-glutamic acid from urine in folic acid deficiency in humans. Proc. Soc. Exptl. Biol. Med. 100, 349-354 (1959). [Pg.241]

Nguyen TV, Andresen BS, Corydon TJ, Ghisla S, Abd-El Razik N, Mohsen AW, Cederbaum SD, Roe DS, Roe CR, Lench NJ, Vockley J. Identification of isobutyryl-CoA dehydrogenase and its deficiency in humans. Mol Genet Metab. 2002 Sep-Oct 77(l-2) 68-79. PubMed citation... [Pg.6]

Najjar and co-workers58 found on diets furnishing only 60 to 90 ig. of riboflavin per day that the urinary excretion (human) was about twice the intake, and the fecal excretion was about 5 to 6 times the intake. This indicates that for certain individuals on certain diets synthesis of riboflavin by intestinal organisms is sufficient to take care of the entire riboflavin needs. The authors conclude that riboflavin may not be a dietary essential in all cases. If this finding is valid, it certainly points to the probability that human needs vary widely because riboflavin deficiencies in human beings have been observed a great many times on many different types of diets. [Pg.199]

Iodine is essential in the mammalian diet to produce the thyroid hormone thyroxine deficiency in humans causes goitre. Collectively, deficiencies of iodine, iron, zinc and vitamin A in humans are thought to be at least as widespread and debilitating as calorie deficiencies (Welch and Graham, 1999). The main source of iodine in soils is oceanic salts rather than parent rock, and so deficiency is most widespread in areas remote from the sea (Fuge, 1996). In principle deficiency is easily corrected with dairy supplements. However in practice this is not always feasible. Addition of iodate to irrigation water has successfully corrected widespread iodine deficiency in parts of China where the usual methods of supplementation had failed (Cao et al., 1994 Jiang et al 1997). However there is not much information on the behaviour of iodine in soil and water systems. [Pg.232]

Taurine deficiency is rare in adult humans but is common in domestic cats, due to poor absorption from tinned catfood. Consequences of taurine deficiency in cats are cardiomyopathy, retinal degradation, reproductive failure in females, developmental abnormalities and impairment of the immune system. It is possible that a chronic deficiency in humans may have similar effects. [Pg.158]

Deficiency in humans is rare because of the widespread availability of pantothenic acid in the usual diet. However, a deficiency of this nutrient can lead to a burning sensation in feet and numb toes. [Pg.628]

There is no record of pantothenic acid deficiency in humans, since all food contains sufficient quantities of this vitamin. Experimentally, however, neurological, gastrointestinal, and cardiovascular symptoms result from a diet lacking in pantothenic acid. [Pg.506]

Bi2 are only about 2 meg, it would take about 5 years for all of the stored vitamin B12 to be exhausted and for megaloblastic anemia to develop if Bi2 absorption were stopped. Vitamin B12 in physiologic amounts is absorbed only after it complexes with intrinsic factor, a glycoprotein secreted by the parietal cells of the gastric mucosa. Intrinsic factor combines with the vitamin Bi2 that is liberated from dietary sources in the stomach and duodenum, and the intrinsic factor-vitamin Bi2 complex is subsequently absorbed in the distal ileum by a highly selective receptor-mediated transport system. Vitamin Bi2 deficiency in humans most often results from malabsorption of vitamin B12 due either to lack of intrinsic factor or to loss or malfunction of the specific absorptive mechanism in the distal ileum. Nutritional deficiency is rare but may be seen in strict vegetarians after many years without meat, eggs, or dairy products. [Pg.735]

Ruel IL, Couture P, Cohn JS, Bensadoun A, Marcil M, Lamarche (2004) Evidence that hepatic lipase deficiency in humans is not associated with proatherogenic changes in HDL composition and metabolism. J Lipid Res 45 1528-1537... [Pg.548]

Holman, R. T, 1973. Essential fatty acid deficiency in humans. In Dietary Lipids and Postnatal Development. C. Galli, G, Jacini, and A. Pecile (Editors). Raven Press, New York, p. 127. [Pg.208]


See other pages where Deficiency in humans is mentioned: [Pg.381]    [Pg.385]    [Pg.28]    [Pg.62]    [Pg.68]    [Pg.88]    [Pg.1117]    [Pg.695]    [Pg.486]    [Pg.1487]    [Pg.200]    [Pg.430]    [Pg.325]    [Pg.678]    [Pg.679]    [Pg.274]    [Pg.127]    [Pg.8]    [Pg.254]    [Pg.278]    [Pg.68]    [Pg.620]    [Pg.481]    [Pg.678]    [Pg.679]    [Pg.337]    [Pg.30]    [Pg.363]    [Pg.386]   


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