Inhibition of propylene glycol stimulated gluconeogenesis by quinolinic acid in the fasting rat

Abstract

Administration of propylene glycol to fasting rats results in an increased rate of hepatic glycogen synthesis, an increased amount of hepatic glycogen, and an increased concentration of serum glucose. Intraperitoneal administration of quinolinic acid gives weak inhibition of these gluconeogenic parameters in control animals, but results in potent inhibition of propylene glycol mediated gluconeogenesis, including rate of synthesis of serum glucose. This inhibition is dose dependent. Nephrectomized rats have an increased sensitivity to quinolinic acid. It is concluded that difficulties in demonstrating inhibition of gluconeogenesis in vivo by quinolinic acid result from rapid renal clearance of the compound and from the relatively small amount of substrate available for the sensitive process. The data suggest that regulation of basal gluconeogenesis is at least partially different from gluconeogenic regulation in the presence of more than minimal amounts of substrate and that quinolinic acid derived from dietary tryptophan may be a physiological regulator of gluconeogenesis.