Effect of Copper Deficiency on Metabolism and Mortality in Rats Fed Sucrose or Starch Diets

Abstract

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.

The Role of Copper as a Modifier of Lipid Metabolism

“…The copper deficient sucrose fed rats had a 3-fold lower hepatic copper level compared to starch-fed copper deficient rats. These results suggested a sucrose-dependent change in copper mobilization or retention within the liver (64). Cardiac abnormalities consistent with copper deficiency were also observed.…”

“…Copper-deficient rats fed a sucrose-based or starchbased diets all had increased plasma cholesterol and lower plasma ceruloplasmin levels, as observed in copper deficiency alone (64). However, feeding sucrose rather than starch greatly enhanced deleterious effects of copper deficiency, such that those animals showed 60% mortality in the 9-week study.…”

“…When this idea is tested in rats by combining high fat and fructose, or low fat and fructose with copper deficiency, liver metabolism is most significantly affected by the fat and fructose combination (28). Sugars mobilize copper from the liver to other tissues (64), possibly causing a change in liver physiology. Recent work also indicates that the mobilization of copper from the liver may be driven by heartspecific copper deficiency (10).…”

Dietary Cu stabilizes brain superoxide dismutase 1 activity and reduces amyloid Aβ production in APP23 transgenic mice

“…This occurrence could be due to a Cu deficiency as observed in the APP transgenic mice strain Tg2576 (19), possibly in conjunction with an age-associated breakdown of metal regulation (19) and the Cu-deficient sucrose-supplemented drinking water. For instance, in rats that were exclusively fed a Cu-deficient sucrose diet (27), an increased mortality had been observed. Moreover, Cu treatment had a modulating effect on brain Cu levels and a normalizing effect on SOD-1 activity in these mice, compared with nontransgenic littermate control mice.…”

Antioxidants status in type 2 diabetic patients in Morocco

“…Cu is a prooxidant and high levels of this trace element may be associated with OS and an increase in LDL oxidation (32). However, a deficiency of Cu may be associated with carbohydrate intolerance and insulin resistance (33). Cu also has insulin-like activity (29).…”