Apolipoprotein B messenger RNA editing in rat liver: Developmental and hormonal modulation is divergent from apolipoprotein A-IV gene expression despite increased hepatic lipogenesis

Y. Inui, A. M.L. Hausman, N. Nanthakumar, S. J. Henning, N. O. Davidson

Research output: Contribution to journalArticlepeer-review

22 Scopus citations

Abstract

Rat hepatic apolipoprotein B (apoB) mRNA editing is regulated developmentally as well as by hormonal and nutritional modulation of hepatic lipogenesis, changes previously associated with coordinate modulation of hepatic apoA-IV gene expression. We have examined the effects of dexamethasone administration on apoB mRNA editing and the expression of other apolipoprotein genes in both neonatal and adult rats. Administration of dexamethasone increased hepatic triglyceride content in neonatal rats and increased hepatic but not intestinal apoA-IV mRNA abundance. However, neither the developmental profile nor the extent of hepatic apoB mRNA editing was changed after hormone administration. Dexamethasone produced a dose-dependent increase in adult hepatic triglyceride content and a coordinate fourfold increase in hepatic but not intestinal apoA-IV mRNA abundance, and hepatic and serum apoA-IV protein concentrations. Immunocytochemical localization revealed apoA-IV to be expressed in hepatocytes around the central vein while dexamethasone treatment produced a dose-dependent appearance of fat-filled hepatocytes throughout the lobule that were immunoreactive for apoA-IV. Despite these changes in hepatic triglyceride accumulation there was no change in the extent of hepatic apoB mRNA editing at any dose of dexamethasone. The data suggest that hormonal and metabolic modulation of hepatic apoB mRNA editing may be independent of factors that modulate apoA- IV gene expression despite alterations in hepatic triglyceride content.

Original languageEnglish
Pages (from-to)1843-1856
Number of pages14
JournalJournal of lipid research
Volume33
Issue number12
StatePublished - 1992

Keywords

  • fatty liver
  • immunocytochemistry
  • triglyceride metabolism

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