Calcium-mobilizing effectors inhibit P-enolpyruvate carboxykinase gene expression in cultured rat hepatocytes

Alfons Valera, Gemma Solanes, Fatima Bosch

Research output: Contribution to journalArticleResearchpeer-review

3 Citations (Scopus)

Abstract

Incubation of primary cultures of hepatocytes from fed and fasted rats with calcium ionophore strongly decreased glucose production from pyruvate. Like insulin, calcium ionophore A23187, phenylephrine, vasopressin, and prostaglandins E2 and F2α caused a significant reduction (50-60%) in basal concentrations of mRNA for P-enolpyruvate carboxykinase (PEPCK), the main regulatory enzyme of gluconeogenesis. Phenylephrine, prostaglandin E2 and calcium ionophore A23187 were also able to counteract the induction of PEPCK gene expression by Bt2cAMP. These effects were similar to those exerted by both vanadate and phorbol ester TPA. The decrease in extracellular calcium by the addition of the calcium-chelating agent EGTA to the incubation medium caused an increase in PEPCK mRNA levels. This effect was additive to that of Bt2cAMP and was counteracted by vanadate. © 1993.
Original languageEnglish
Pages (from-to)319-324
JournalFEBS Letters
Volume333
Issue number3
DOIs
Publication statusPublished - 1 Nov 1993

Keywords

  • Calcium ionophore A23187
  • Gene expression
  • Insulin
  • P-enolpyruvate carboxykinase
  • Phenylephrine

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