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Defects of Copper Deficiency in Rats Are Modified by Dietary Treatments that Affect Glycation^1,2,

U.S. Department of Agriculture, Agricultural Research Service, Grand Forks Human Nutrition Research Center ^* Department of Physiology, University of North Dakota, Grand Forks, ND 58202

We examined the hypothesis that nonenzymatic glycosylation of proteins (glycation) contributes to the defects of copper deficiency. We studied copper-adequate and -deficient rats while altering two factors known to affect glycation: type of dietary carbohydrate and amount of food intake. Copper deficiency caused cardiac enlargement and anemia, decreased erythrocyte osmotic fragility, enhanced heart lipid peroxidation, increased the percentage of glycated hemoglobin (Hb A₁) and reduced staining of lens crystallins on SDS-PAGE gels (suggestive of glycation). Increasing dietary sucrose reduced organ copper concentration, exacerbated the rise in Hb A₁ and worsened the anemia caused by copper deficiency. Food restriction ameliorated heart and erythrocyte defects, reduced the percentage of glycated hemoglobin and heart peroxidation and also improved heart and liver copper status in copper-deficient rats. These findings indicate that copper deficiency enhances glycation and that sucrose may exacerbate some defects of copper deficiency by enhancing glycation. Inhibition of defects of copper deficiency by food restriction suggests that glycation and/or peroxidation may contribute to those defects.

KEY WORDS: • glycation • food restriction • rats • copper • peroxidation

¹ Presented in part at Experimental Biology 94, April 1994, Anaheim, CA [Saari, J. T. & Bode, A. M. (1994) Influence of factors affecting glycation on defects of dietary copper deficiency. FASEB J. 8: A710 (abs. 4121)].

² The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 USC section 1734 solely to indicate this fact.

³ To whom correspondence should be addressed.

Manuscript received 20 March 1995. Revision accepted 18 July 1995.