1987 Volume 28 Issue 3 Pages 319-323
Decreased insulin binding has been reported in various liver diseases. But its mechanism could not be clearly delineated. To address this problem, IRI levels before or after 10min of IV glucose load, glucose tolerance curve and insulin binding to liver 40, 000g pellets were measured in rats with normal, CCl4 induced acute and chronic liver injury. IRI levels before or after IV glucose load were highest in acute liver injury, higher in chronic liver injury than in normal. Abnormal glucose tolerance was suspected in acute and chronic liver injury after IV glucose load. Specific insulin binding was lowest in acute liver injury, lower in chronic liver injury than in normal. Scatchard plots revealed that its decrease in acute and chronic liver injury was mainly due to reduced binding sites. From these results, we conclude that the decreased insulin binding exists probably as a consequence of hyperinsulinemia.