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

¹ Department of Pharmacology, New York University School of Medicine, New York, and Biology Department, Brookhaven National Laboratory, Upton, New York

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.

Key Words: insulin and hepatic glycogenolysis • insulin and glucose uptake by liver • insulin and incorporation of plasma glucose into liver glycogen • stimulation of glycogen synthesis by insulin

Submitted on April 8, 1964

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