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Apolipoprotein A‐I, A‐IV and E synthesis in the liver of copper‐deficient rats
Author(s) -
Nassir Fatiha,
Mazur Andrzej,
Gueux Elyett,
Sérougne Colette,
Rayssiguier Yves
Publication year - 1994
Publication title -
lipids
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.601
H-Index - 120
eISSN - 1558-9307
pISSN - 0024-4201
DOI - 10.1007/bf02538918
Subject(s) - lipidology , clinical chemistry , copper , medicine , chemistry , apolipoprotein b , endocrinology , biochemistry , cholesterol , organic chemistry
Copper deficiency induces hypercholesterolemia in the rat. This hypercholesterolemia is mainly due to an increase in apo E‐rich high density lipoproteins (HDL 1 ). The present study was undertaken to determine whether the HDL increase could be explained by altered low‐molecular weight apolipoprotein (apo) synthesis in the liver. The effect of copper deficiency on apo A‐I, apo A‐IV and apo E concentrations in plasma, as well as on respective mRNA levels and synthesis in the liver, were therefore investigated. We observed that the increased HDL 1 levels in the plasma of copper‐deficient rats were associated with a significant rise in plasma apo E concentrations; however, plasma apo A‐I and apo A‐IV concentrations remained unchanged. Liver apo synthesis and respective apo mRNA levels were not significantly altered in copper‐deficient animals when compared to control rats. No changes in apo E mRNA levels in various tissues from copper‐deficient, as compared to control rats, were noted. Based on the data obtained, it was concluded that the observed changes in plasma lipoprotein and apo concentrations are not related to changes in low‐molecular weight apo synthesis in the liver. The mechanisms of the impaired catabolism of HDL 1 should be further evaluated to possibly explain the observed increase in this fraction in copper‐deficient rats.