Abstract
To clarify the mechanism of hyperinsulinemia often encountered in chronic liver diseases, the activity of Glutathione-Insulin Transhydrogenase (GIT) as insulin degrading enzyme was measured in rat liver.
Experimentally, liver cirrhosis was produced in female Wistar rats by subcutaneous injection of CCl4 (1.5ml/kg) twice a week for 12 weeks, and diabetic rats were produced by intravenous injection of streptozotocin (65mg/kg).
The rats were decapitated in fasting state and at 30 min. after 3g/kg of oral glucose administration and 10, 000×g supernatant of liver homogenate was used as enzyme preparation. The GIT activity was measured by counting radioactivity of 125I-insulin, degraded by GIT with the use of 15% TCA.
Fasting blood glucose levels were significantly decreased in cirrhotic rats, whereas these were elevated in diabetic rats.
Plasma IRI levels were higher in cirrhotic rats in general, whereas decreased IRI levels were observed in diabetic rats. However, GIT activity was significantly enhanced in cirrhotic rat liver, whether expressed per gm. of liver or mg protein. Furthermore the enzyme activity was slightly reduced in the diabetic rat liver.
Thus, GIT activity appears to be induced by the elevated plasma insulin levels as seen in liver cirrhosis.
