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A copper deficient diet prevents hepatic copper accumulation and dysfunction in Long-Evans Cinnamon (LEC) rats with an abnormal copper metabolism and hereditary hepatitis

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Abstract

Long-Evans Cinnamon (LEC) rats that develop spontaneous hepatitis due to an inherently abnormal Cu metabolism have recently been established. This investigation concerns the effects of a Cu-deficient diet on the Cu metabolism linked to hepatic injury in LEC rats. The hepatic Cu concentration at 30 days after birth was 94±4 Cu μg/g liver in LEC rats, whereas that of Fischer rats at the same age was 7±1 Cu μg/g. From 30 days after birth, all rats were fed a semisynthetic diet with two different levels of Cu, 0.5 or 30 μg/g food, for 35 days. In LEC rats fed a Cu-deficient diet (0.5 μg/g), the hepatic Cu concentration was 39±7 μg/g. The Cu-normal diet (30 μg/g) LEC group had a concentration of 357±15 μg/g in the hepatic Cu. The group had significantly higher aspartate aminotransferase (ASAT), alanine aminotransferase (ALAT) and γ-glutamyl transferase (GGT) levels than did the LEC rats given the Cu-deficient diet. These results suggest that the occurrence of acute hepatitis in LEC rats can be prevented by feeding the animals a Cu-deficient diet.

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Sugawara, N., Sugawara, C. A copper deficient diet prevents hepatic copper accumulation and dysfunction in Long-Evans Cinnamon (LEC) rats with an abnormal copper metabolism and hereditary hepatitis. Arch Toxicol 69, 137–140 (1994). https://doi.org/10.1007/s002040050149

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  • DOI: https://doi.org/10.1007/s002040050149

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