Renal cortical and hepatic phosphoenolpyruvate carboxylase in the diabetic rat: Effect of acid-base status

Abstract

Phosphoenolpyruvate (PEP) carboxylase activity was determined in renal cortex and liver from diabetic rats given NaCl (acidotic) or NaHCO 3 (nonacidotic) and in normal animals given ammonium chloride or NaHCO 3. When compared with control animals, diabetic acidosis increased PEP carboxylase activity in both liver and renal cortex. Sodium bicarbonate administration to diabetic animals returned renal cortical enzyme activity to control levels, but failed to influence enzyme activity in liver. The increase in renal cortical PEP carboxylase activity following induction of acidosis with ammonium chloride in normal animals or in insulin-treated diabetic animals was similar, for any given reduction in plasma carbon dioxide, to that found during spontaneous diabetic acidosis. It is concluded that the increase in hepatic PEP carboxylase present during diabetes is secondary to the defect in carbohydrate metabolism and independent of the changes in acid-base status. In renal cortex, on the other hand, the increase in PEP carboxylase during diabetes is secondary to the associated acidosis and independent of the defect in carbohydrate metabolism.