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Dietary fructose exacerbates the cardiac abnormalities of copper deficiency in rats

  • Robert S. Redman
    Correspondence
    Correspondence to: Robert S. Redman, D.D.S., Ph.D., Oral Pathology Research Laboratory (151-I), Veterans Administration Medical Center, 50 Irving Street, NW, Washington, DC 20422, U.S.A. Telephone: (202) 745-8490.
    Affiliations
    Oral Pathology Research Laboratory, Veterans Administration Medical Center, Washington, DC, U.S.A.

    Georgetown University Medical and Dental Schools, Washington, DC, U.S.A.
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  • Meira Fields
    Affiliations
    Georgetown University Medical and Dental Schools, Washington, DC, U.S.A.

    Vitamin and Mineral Nutrition, Beltsville Human Nutrition Research Center, Agricultural Research Service, United States Department of Agriculture, Beltsville, MD, U.S.A.
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  • Sheldon Reiser
    Affiliations
    Carbohydrate Nutrition Research Laboratories, Beltsville Human Nutrition Research Center, Agricultural Research Service, United States Department of Agriculture, Beltsville, MD, U.S.A.
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  • J.Cecil Smith Jr.
    Affiliations
    Vitamin and Mineral Nutrition, Beltsville Human Nutrition Research Center, Agricultural Research Service, United States Department of Agriculture, Beltsville, MD, U.S.A.
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      Abstract

      Copper deficiency has been shown to result in severe cardiovascular lesions in several species of animals. The principal carbohydrate in the copper-deficient diet most often used with rats is sucrose, which is known to have adverse effects on carbohydrate and lipid metabolism and thus may contribute to cardiovascular disorders. These observations prompted experiments in which starch and fructose were substituted for sucrose in a copper-deficient diet, to see if the effects of the copper deficiency might be modified. In the hearts from rats fed copper-deficient diets with fructose or sucrose, there was marked, mostly ventricular hypertrophy, and mild to severe myocardial inflammation, degeneration, and fibrosis. Aneurysm of the left ventricle and pericarditis also were common. Hearts from the starch, copper-deficient groups were much less hypertrophic, and very few were affected by myocardial inflammation, degeneration, or fibrosis. Defects of elastin or other structures were not observed in the aortas or pulmonary or coronary arteries of any specimens.

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