|Bode, Ann - UNIV OF NORTH DAKOTA|
Submitted to: Journal of Nutrition
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: July 18, 1995
Publication Date: N/A
Interpretive Summary: Some interactions among nutrients in the body may exert adverse effects on tissues and organs and thus promote the development of some types of diseases. When undesirable binding of sugars to proteins (glycation) occurs, the proteins are damaged and their function is impaired. Similarly, the body's use of oxygen can result in the production of highly reactive chemical substances (free radicals) that damage body structures and impair organ functions. Both of these processes have been implicated in defects caused by dietary copper deficiency. To further examine the role of these processes in damage caused by copper deficiency, we treated copper-deficient rats in ways expected to alter glycation and then measured the resultant effects of these treatments on indices of glycation and free radical damage and on defects caused by copper deficiency. Feeding of high sucrose diets, which enhances glycation, exaggerated some of the defects of copper deficiency, but did not affect free radical damage. Restricting food intake, which reduces glycation, reduced some of the defects of copper deficiency and also reduced free radical damage. These findings indicate that both undesirable binding of sugar to protein and free radical damage are involved in the defects associated with dietary copper deficiency. Because both excessive binding of sugars to protein and free radical damage are associated with defects of diabetes and aging, copper deficiency may be a model for these two conditions.
Technical Abstract: The hypothesis that nonenzymatic glycosylation of proteins (glycation) contributes to the defects of copper deficiency was examined. Copper- adequate and -deficient rats were studied 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 percent 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 percent 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.