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Intestinal Absorption and Excretion of Zinc in Streptozotocin-Diabetic Rats as Affected by Dietary Zinc and Protein¹

U.S. Department of Agriculture, Agricultural Research Service, Grand Forks Human Nutrition Research Center and Department of Biochemistry and Molecular Biology, University of North Dakota, Grand Forks, ND 58202

⁶⁵Zn was used to examine the effects of dietary zinc and protein on true zinc absorption and intestinal excretion of endogenous zinc by an isotope dilution technique in streptozotocin-diabetic and control rats. Four groups each of diabetic and control rats were fed diets containing 20 ppm Zn, 20% egg white protein (HMHP); 20 ppm Zn, 10% egg white protein (HMLP); 10 ppm Zn, 20% egg white protein (LMHP); and 10 ppm Zn, 10% egg white protein (LMLP). Measurement of zinc balance was begun 9 d after an i.m. injection of ⁶⁵Zn. True zinc absorption and the contribution of endogenous zinc to fecal zinc excretion were calculated from the isotopically labeled and unlabeled zinc in the feces, duodenum and kidney. Results from the isotope dilution study indicated that diabetic rats, but not control rats, absorbed more zinc from 20 ppm zinc diets than from 10 ppm zinc diets and that all rats absorbed more zinc from 20% protein diets than from 10% protein diets. Furthermore, all rats excreted more endogenous zinc from their intestines when dietary zinc and protein levels resulted in greater zinc absorption. In diabetic and control rats, consuming equivalent amounts of zinc, the amount of zinc absorbed was not significantly different, but the amount of zinc excreted by the intestine was less in the diabetic rats. Decreased intestinal excretion of endogenous zinc may be a homeostatic response to the increased urinary excretion of endogenous zinc in the diabetic rats and may also lead to the elevated zinc concentrations observed in some organs of the diabetic rats.

KEY WORDS: • zinc • absorption • excretion • diabetes • homeostasis

¹ Supported in part by the U.S. Department of Agriculture Cooperative Agreement No. 58-519B-2-1189.

Manuscript received 21 December 1984. Revision accepted 23 May 1985.