Copper deficiency can cause cardiovascular lesions in experimental animals. Previous experiments have shown that the biochemical and itDrphologic lesions induced by deprivation of dietary copper can be suppressed by feeding diets containing starch or can be magnified by a high sucrose diet. In a recent study it was found that the more severe signs of copper deficiency in rats fed sucrose as compared to starch were due to the fructose moiety of sucrose. Although fructose as compared to starch markedly enhanced the symptoms of copper deficiency, the possibility that an effect of dietary carbohydrates due to the nature of the simple carbohydrate (fructose vs glucose) cannot be excluded. The present study was designed to determine if the severity of copper deficiency in rats fed sucrose as compared to starch is due to the glucose as well as the fructose moiety of sucrose. This portion of the study assessed the morphologic changes in aortas of seventy weanling male rats who were fed, for 9 weeks, copper deficient or copper supplemented diets containing either 62% starch, fructose or glucose. The starch-fed copper supplemented group served as the most normal controls. Rats were sacrificed after 9 weeks of dietary treatments. Copper deficiency was verified by reduced serum ceruloplasmin activity and serum and hepatic copper concentration.
Idiopathic Copper Deficiency Induced Myeloneuropathy
