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Zinc: Human Nutrition and Metabolic Effects

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▸Requests for reprints should be addressed to Ananda S. Prasad, M.D., Department of Medicine, Wayne State University School of Medicine, 1400 Chrysler Expressway, Detroit, Mich. 48207

Detroit and Allan Park, Michigan

Ann Intern Med. 1970;73(4):631-636. doi:10.7326/0003-4819-73-4-631
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A nutritional deficiency of zinc in man which occurs in the Middle East produces severe growth retardation, hypogonadism, roughened skin, general lethargy, and an oral glucose tolerance test suggestive of delayed absorption. Metabolically induced zinc deficiency has been noted in patients with repeated infections, cirrhosis of the liver, and malabsorption. Stunted growth and lack of sexual development are main manifestations in puberty, but poor wound healing may be the primary feature in older persons. Experimentally, zinc-deficient rats show susceptibility to infections and lymphocytopenia. Therefore, the testicular atrophy, susceptibility to infections, and lymphocytopenia that are commonly seen in patients with liver cirrhosis may be attributable to zinc deficiency. Fetal abnormalities in offspring of zinc-deficient rats and chicks are not yet known to occur in man. Impaired behavior and decreased learning ability that occur in zinc-deficient rats are manifestations needing evaluation in zinc-deficient human subjects. Experimental observations in animals indicate that cell zinc controls physiological processes by regulating the activities of zinc-dependent enzymes. The precise role of zinc in enzymatic functions; formation or degradation of RNA, DNA, and proteins; and in cell division remains to be elucidated.





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