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Increased hepatic synthesis and accumulation of plasma apolipoprotein B100 in copper‐deficient rats does not result from modification in apolipoprotein B mRNA editing
Author(s) -
Nassir Fatiha,
Giani Federico,
Mazur Andrzej,
Rayssiguier Yves,
Davidson Nicholas O.
Publication year - 1996
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/bf02522931
Subject(s) - apolipoprotein b , clinical chemistry , messenger rna , lipidology , chemistry , lipoprotein , medicine , endocrinology , primer extension , microbiology and biotechnology , biochemistry , biology , cholesterol , gene
Abstract Experimentally induced copper deficiency in the rat results in increased plasma apolipoprotein B100 (apo B100) concentration in association with increased hepatic apo B100 synthesis. This enhancement of apo B100 synthesis and plasma accumulation accounts for the rise of plasma low density lipoprotein in these animals. In the present study, we have investigated if the selective increase in hepatic apo B100 synthesis is accounted for by changes in apo B mRNA editing. Reverse transcription coupled with polymerase chain reaction amplification and primer extension analysis of apo B cDNA revealed no differences in apo B mRNA editing in either the liver or small intestine between control and copper‐deficient rats. We speculate that the increase in apo B100 synthesis in the liver of copper‐deficient rats reflects posttranslational alterations in gene expression accompanying changes in very low density lipoprotein assembly and secretion.