Role of insulin as a portal factor in maintaining the viability of liver.

The subcutaneous administration of insulin did not induce a significant effect on oxidative phosphorylation of the mitochondria from normal rat liver. However, in rats subjected to ligation of a branch of portal vein, the phosphorylative activity of the mitochondria from the ligated lobe deprived of portal blood fell rapidly and at 12 hours decreased to approximately 50% of nomal liver mitochondria. After the insulin administration, the phosphorylative activity of the mitochondria from ligated lobe was rapidly stimulated within 30 minutes, reached the maximal level of normal liver mitochondria at 2 hours (p < 0.005) and then fell to subnormal levels. The respiratory control ratio, state 3 respiration and P/O ratio remarkably increased in parallel with an increase of phosphorylative activity. The contents of respiratory enzymes making up ATP remained unchanged. Considering the previous report that a factor, which is capable of stimulating oxidative phosphorylation of the liver mitochondria, is present in portal blood, it is suggested that insulin may play an important role in the mechanism by which the portal blood controls mitochondrial metabolism.