APOLIPOPROTEIN-B MESSENGER-RNA EDITING IS PRESERVED IN THE INTESTINE AND LIVER OF ZINC-DEFICIENT RATS

Apolipoprotein B (apo B) mRNA editing is a site-specific, post-transcr iptional cytidine deamination reaction that generates apo B48 in the m ammalian small intestine and in the liver of certain animals. This rea ction is mediated by an enzyme complex that includes the catalytic sub unit apobec-1, a zinc-dependent cytidine deaminase. To determine the i mportance of zinc status to apo B mRNA editing in vivo, we examined th e effects of experimentally induced zinc deficiency in rats upon hepat ic and serum lipid levels and several indices of apo B gene expression . Rats were either given unlimited access to or were pair-fed a semipu rified zinc-supplemented (30 mg Zn/kg) diet or were fed a zinc-deficie nt diet (similar to 1 mg Zn/kg) for 17 d. Significant differences were detected in the ratio of serum apo B100/B48 in the unlimited access, zinc-supplemented group compared with either zinc-deficient rats or pa ir-fed controls. There were no alterations in hepatic triglyceride and cholesterol concentrations, hepatic apo B mRNA abundance or apo B mRN A editing in either the small intestine or liver. Taken together, thes e data suggest that the altered ratios of serum apo B isomorphs seen i n zinc deficiency are not mediated through changes in hepatic or intes tinal apo B mRNA editing.