The purpose of this investigation was to study the interaction between copper and dietary carbohydrates on clinical and enzymatic indices associated with copper deficiency. Copper deficiency was produced in rats by feeding diets adequate in all nutrients including selenium and chromium, but marginal in copper ( 1.2 pg/g diet) containing 62% of either starch, fructose,or glucose. During the fifth week, the fmctose of the copper-deficient diet (20 rats) was replaced by either starch (10 rats) or by glucose (10 rats). The experiment was terminated after 1 1 weeks.Copper deficiency in rats fed fructose significantly lowered body weight and hematocrit, but increased liver weight, blood urea nitrogen, ammonia, cholesterol, and triglycerides when compared to rats fed starch or glucose. The copper metalloenzyme, superoxide dismutase, the selenoenzyme, glutathione peroxidase, and hepatic ATP were decreased in the copper-deficient rats fed fructose as compared to copper-deficient rats fed starch or glucose. These results indicate that fructose may be the dietary component which has a deleterious effect on copper and selenium status. Changing the type of dietary carbohydrate in copper-deficient rats from fructose to either starch or glucose ameliorated the severity of the deficiency. The protective effects were more pronounced with starch than with glucose. 30

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The present study was designed to determine if the more severe copper deficiency in rats fed sucrose and fructose, as compared to starch, is due to a specific effect of the fructose or to a nonspecific effect of any simple carbohydrate. Seventy weanling male rats were fed, for 9 wk, copper-deficient diets or copper-supplemented diets containing either 62% starch, fructose, or glucose. Decreased hematocrit, serum copper, and ceruloplasmin concentrations but increased heart and liver weights, total liver lipid, and hepatic iron concentrations were found in all copper-deficient rats regardless of the dietary carbohydrate. Feeding rats the high glucose diet decreased plasma albumin and liver glycogen but increased blood urea nitrogen when compared to rats fed starch. However, rats fed fructose generally exhibited a more severe copper deficiency as compared to rats fed either starch or glucose. The severity was characterized by lower (p less than 0.05) body weight, liver glycogen, hematocrit, serum copper, and albumin. Conversely, liver and heart weights, blood urea nitrogen, and plasma glutamic oxaloacetic transaminase were higher (p less than 0.05). Plasma cholesterol was increased by copper deficiency only in rats fed fructose or glucose. During the study, 17 of the 40 rats fed copper-deficient diets died; 66% of those fed fructose, 26% fed glucose, and 30% fed starch. These results suggest that the fructose moiety of sucrose is responsible for the increased severity of copper deficiency in rats fed sucrose as compared to starch.

Copper deficiency was induced in rats by feeding sucrose or starch diets deficient in copper. Copper-deprived rats fed either diet exhibited decreased plasma ceruloplasmin concentration and increased plasma cholesterol. Glucose homeostasis and utilization was impaired both in vivo and in vitro. Oral glucose tolerance was impaired, insulin binding decreased, and CO2 formation and lipogenesis from [U-14C]glucose were decreased. Feeding sucrose but not starch diets deficient in copper magnified the copper deficiency and resulted in 60% mortality. Although both deficient diets contained the same concentration of copper, the hepatic copper concentration of rats fed sucrose was reduced nearly threefold compared to rats fed starch. Reduced epididymal fat pad, increased liver weight, reduced blood hemoglobin and a marked hypertrophy of the heart with gross deformities as well as histopathologic changes were noted only in those rats fed the copper-deficient sucrose diet. The biochemical lesions induced by deprivation of copper can be suppressed by feeding diets containing starch or can be magnified by high sucrose intake.