Effects of insulin on liver glycogen synthesis and breakdown in the dog

Abstract

Glucose-C14 was given intravenously in trace amount, as an initial dose followed by continuous infusion, to measure glucose-C12 release by the liver, and total glucose uptake from plasma by the tissues. The glycogen content of liver and the C14 incorporated into the glycogen and the nonglycogen constituents of liver were measured by analysis of percutaneous biopsy samples. Glucose 6-C14 was used to show that direct uptake and conversion to liver glycogen (without passage through three carbon intermediates) of tagged blood glucose molecules was the source of almost all the C14 of glycogen Insulin infusion at 0 1–0.2 U/kg per hr, iv, along with glucose to limit hypoglycemia, stopped glycogen loss, decreased glucose-C12 release, increased glucose uptake from the plasma by the tissues and brought about the incorporation of plasma glucose-C14 units into liver glycogen. Incorporation of C14 into the nonglycogen constituents of the liver was increased much less. Glucose infusion, presumed to stimulate endogenous insulin secretion, produced similar effects. In earlier periods of insulin infusion the outstanding hepatic effects were decreases in glycogen loss and glucose-C12 release. In later periods the outstanding further effect was a great increase in the use of plasma glucose-C14 for liver glycogen synthesis.