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Tissue Distribution and Excretion of Copper-67 Intraperitoneally Administered to Rats Fed Fructose or Starch

J. Holbrook^*, M. Fields^1,, J. Cecil Smith, Jr.^*, S. Reiser^* and Los Alamos Medical Research Group

^* Vitamin and Mineral Nutrition Laboratory and Carbohydrate Nutrition Laboratory, Beltsville Human Nutrition Research Center, Agricultural Research Service, U.S. Department of Agriculture, Beltsville, MD 20705 Georgetown University Medical School, Washington, DC 20007 Los Alamos National Laboratory, Los Alamos, NM 87545

It has been suggested that impaired gut absorption of copper is the cause of the exacerbated copper deficiency signs in rats fed fructose when compared to rats fed starch. The present study was designed to examine how rats fed fructose or starch diets, either copper-deficient or supplemented, distributed and excreted ⁶⁷Cu when the isotope was administered i.p. Intraperitoneal administration was chosen in an effort to circumvent primary gut absorption as a factor in the metabolism of ⁶⁷Cu. After 7 wk of dietary treatment, rats received an i.p. injection of ⁶⁷Cu and were placed in metabolic cages for 4 d. Regardless of dietary carbohydrate, copper-deficient rats retained similar levels of radioactivity in various tissues and excreted similar amounts of ⁶⁷Cu in feces and urine. This similarity in copper metabolism in copper-deficient rats fed either fructose or starch when the gut was circumvented for isotope administration suggests that the gut could be responsible, at least in part, for the exacerbated signs associated with the copper deficiency in rats fed fructose. The possibility is discussed that alterations in metabolism may increase the requirement for copper when fructose is the main dietary carbohydrate.

KEY WORDS: • copper • fructose • starch • copper-67 • retention • excretion

¹ To whom reprint requests should be addressed: Dr. Meira Fields, USDA, ARS, BHNRC, Vitamin and Mineral Nutrition Laboratory, Beltsville, MD 20705.

Manuscript received 18 September 1985. Revision accepted 23 December 1985.