[Kinetic studies of protein kinase A in rat liver during early sepsis]

Sepsis-induced glucose dyshomeostasis has been characterized by an initial hyperglycemia followed by a progressive hypoglycemia. It is well known that the liver plays a predominant role on regulating the homeostatic level of blood glucose. Furthermore, recent studies indicate that protein kinase A, activated by c-AMP, contributes to the role of glycagon in glucogenolysis and glyconeogenesis. Kinetic studies of protein kinase were completed. During late sepsis, in order to further understand the pathophysiology of hepatic glucose disturbances during sepsis. This study investigates the role of protein kinase A in the liver regulating carbohydrate metabolism during early sepsis. The work was performed by using an animal septic model, induced by cecal ligation and puncture (CLP) operation. Through the measurement of blood sugar, a two phase change in sugar level was found. That is, blood sugar significantly increased at 4.5 hrs after CLP operation (p < 0.05) and then significantly decreased at 18 hrs (p < 0.01). In the kinetic studies of protein kinase A, the results showed that, during early sepsis, the activities of both type I (eluted at low ionic strength) and type II (eluted at high ionic strength) protein kinase A were unchanged. Moreover, the kinetic parameters, Vmax and S0.5, of protein kinase A showed no significant difference between two groups. As such, it is suggested that hyperglycemia during early sepsis is not connected to the regulation of protein kinase A.