Alcohol consumption mimics the effects of a high-fructose, low-copper diet in rats.

The consumption of a high-fructose diet that is inadequate in copper produces numerous pathologies which eventually lead to the mortality of the animals. In contrast, the consumption of a high-starch diet that is inadequate in copper does not produce abnormalities and the animals survive. Ethanol has been chosen as an agent to mimic the fructose effect in copper deficiency. The administration of 20% ethanol in the drinking water of rats fed a starch-based diet that was inadequate in copper resulted in a depressed growth rate, anemia, pancreatic atrophy, and heart hypertrophy. All these signs were similar to the signs exerted by fructose feeding when it was combined with copper deficiency. Polyol pathway in the liver and kidney was affected by both ethanol and fructose consumption. Ethanol did not aggravate the signs associated with copper deficiency in rats fed fructose, but it exacerbated the signs associated with copper deficiency in rats fed starch. Certain metabolic pathways that are unique for fructose and ethanol may be responsible for the exacerbation of copper deficiency.