DEFECTS OF COPPER DEFICIENCY IN RATS ARE MODIFIED BY DIETARY TREATMENTS THAT AFFECT GLYCATION

We examined the hypothesis that nonenzymatic glycosylation of proteins (glycation) contributes to the defects of copper deficiency. We studi ed copper-adequate and -deficient rats while altering two factors know n to affect glycation: type of dietary carbohydrate and amount of food intake. Copper deficiency caused cardiac enlargement and anemia, decr eased erythrocyte osmotic fragility, enhanced heart lipid peroxidation , increased the percentage of glycated hemoglobin (Hb A(1)) and reduce d staining of lens crystallins on SDS-PAGE gels (suggestive of glycati on). Increasing dietary sucrose reduced organ copper concentration, ex acerbated the rise in Hb A(1) and worsened the anemia caused by copper deficiency. Food restriction ameliorated heart and erythrocyte defect s, reduced the percentage of glycated hemoglobin and heart peroxidatio n and also improved heart and liver copper status in copper-deficient rats. These findings indicate that copper deficiency enhances glycatio n and that sucrose may exacerbate some defects of copper deficiency by enhancing glycation. Inhibition of defects of copper deficiency by fo od restriction suggests that glycation and/or peroxidation may contrib ute to those defects.