A copper deficient diet prevents hepatic copper accumulation and dysfunction in Long-Evans Cinnamon (LEC) rats with an abnormal copper metabolism and hereditary hepatitis.
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 micrograms/g liver in LEC rats, whereas that of Fischer rats at the same age was 7 +/- 1 Cu micrograms/g. From 30 days after birth, all rats were fed a semisynthetic diet with two different levels of Cu, 0.5 or 30 micrograms/g food, for 35 days. In LEC rats fed a Cu-deficient diet (0.5 microgram/g), the hepatic Cu concentration was 39 +/- 7 micrograms/g. The Cu-normal diet (30 micrograms/g) LEC group had a concentration of 357 +/- 15 micrograms/g in the hepatic Cu. The group had significantly higher aspartate aminotransferase (ASAT), alanine aminotransferase (ALAT) and gamma-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.
Sugawara
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N
Department of Public Health, School of Medicine, Sapporo Medical University, Hokkaido, Japan.
Sugawara
C
C
D000818:Animals; D001646:Bile; D003300:Copper / Q000032:analysis / Q000172:deficiency* / Q000378:metabolism; D004032:Diet; D006520:Hepatitis, Animal / Q000151:congenital* / Q000503:physiopathology; D008099:Liver / Q000737:chemistry*; D008297:Male; D051381:Rats; D011916:Rats, Inbred F344
D003300:Copper