Decrease of liver protein kinase C in streptozotocin-induced diabetic rats and restoration by vanadate treatment

Effects of streptozotocin-induced diabetes and administration of the insulinmimetic agent, vanadate in rats on the liver protein kinase C-induced phosphorylation of exogenous C (Histone III-S) and endogenous substrates were investigated. Diabetes caused a significant fall (40-60%) in liver cytosolic protein C activity measured using both types of substrates. Vanadate treatment for a period of 5 weeks restored them to normal levels. Phosphorylation of cytosolic target proteins for protein kinase C followed a similar pattern in response to diabetes and vanadate. These treatments had no effect on particulate protein kinase C activity. Vanadate also had no effect in normal livers with respect to the protein kinase C system.