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Effect of Copper Deficiency on Metabolism and Mortality in Rats Fed Sucrose or Starch Diets

Meira Fields^1,*,,, Renato J. Ferretti, J. Cecil Smith, Jr. and Sheldon Reiser

^* University of Maryland, College Park, MD 20742 and U.S. Department of Agriculture (USDA), Beltsville Human Nutrition Research Center, Vitamin and Mineral Nutrition Laboratory, Beltsville, MD 20705 and USDA, Beltsville Human Nutrition Research Center, Carbohydrate Nutrition Laboratory, Beltsville, MD 20705

Copper deficiency was induced in rats by feeding sucrose or starch diets deficient in copper. Copper-deprived rats fed either diet exhibited decreased plasma ceruloplasmin concentration and increased plasma cholesterol. Glucose homeostasis and utilization was impaired both in vivo and in vitro. Oral glucose tolerance was impaired, insulin binding decreased, and CO₂ formation and lipogenesis from [U-¹⁴C]glucose were decreased. Feeding sucrose but not starch diets deficient in copper magnified the copper deficiency and resulted in 60% mortality. Although both deficient diets contained the same concentration of copper, the hepatic copper concentration of rats fed sucrose was reduced nearly threefold compared to rats fed starch. Reduced epididymal fat pad, increased liver weight, reduced blood hemoglobin and a marked hypertrophy of the heart with gross deformities as well as histopathologic changes were noted only in those rats fed the copper-deficient sucrose diet. The biochemical lesions induced by deprivation of copper can be suppressed by feeding diets containing starch or can be magnified by high sucrose intake.

KEY WORDS: • copper • sucrose • starch • insulin • lipogenesis • cholesterol • ceruloplasmin • heart histopathology • mortality

¹ Visiting scientist with University of Maryland, College Park, Maryland 20742.

Manuscript received 28 October 1982.

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