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American Journal of Clinical Nutrition, Vol 24, 411-415, Copyright © 1971 by The American Society for Clinical Nutrition, Inc.
1 Fellow, Division of Gastroenterology, Rhode Island Hospital, Providence, Rhode Island 02903
2 Associate Professor of Medical Sciences, Brown University, Providence, Rhode Island; Director, Division of Gastroenterology, Rhode Island Hospital; and Consultant in Gastroenterology, Providence Veterans Administration Hospital
Four groups of rats were raised on: 1) a control diet (27% casein and 28 mg/100 g iron), 2) a protein-deficient diet (5% casein and 37 mg/100 g iron), 3) an iron-deficient diet (27% casein and 0 iron), and 4) a combined protein- and iron-deficient diet (5% casein and 0 iron). The rats on the protein-deficient diet developed only mild anemia while the iron-deficient rats became severely anemic. The rats on the combined deficiency diet became only moderately anemic, but had no stainable iron in the bone marrow. Disaccharidase (lactase, sucrase, maltase) activity in the protein-deficient and iron-deficient rats was not significantly different from that of the normal rats. However, the disaccharidase levels in the iron-deficient rats were markedly diminished. These results do not indicate that protein deprivation will result in an acquired lactase deficiency.
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