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Calcium‐mobilizing effectors inhibit P‐ enol pyruvate carboxykinase gene expression in cultured rat hepatocytes
Author(s) -
Valera Alfons,
Solanes Gemma,
Bosch Fatima
Publication year - 1993
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(93)80679-o
Subject(s) - calcium , phosphoenolpyruvate carboxykinase , egta , gluconeogenesis , endocrinology , ionophore , medicine , chemistry , vanadate , biochemistry , biology , extracellular , metabolism , enzyme
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 E 2 and F 2α caused a significant reduction (50–60%) in basal concentrations of mRNA for P‐ enol pyruvate carboxykinase (PEPCK), the main regulatory enzyme of gluconeogenesis. Phenylephrine, prostaglandin E 2 and calcium ionophore A23187 were also able to counteract the induction of PEPCK gene expression by Bt 2 cAMP. 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 Bt 2 cAMP and was counteracted by vanadate.