早期敗血症時大白鼠肝中蛋白激酶A之動力探討

於體人醣類之代謝之過程，其中最主要的機轉是藉由各種蛋白激酶以磷酸化和去磷酸化方式對細胞表面接受器蛋白(receptor protein)進行共使或修飾。而肝臟對醣類之代謝機制之一是藉賀爾蒙作用於接受器上，進而改變c-AMP所活化之蛋白激酶A的活性，以調節正常細胞之醣類代謝功能。於敗上症時造成體內血糖值的改變，起先血糖於早期4.5hr時呈意義的上升，而於晚期18ht時卻呈顯著意義下降。本實以盲腸結紮並螫孔之手術（簡稱CLP）發老鼠敗血症之發生，進而探討敗血症早期時肝臟中的蛋白激酶A於醣類代所扮演的角色。結果顯示敗血症早期時，肝臟中蛋白激酶A之type I（由低離子強度時所洗出）與type II（由高離子強度時所洗出）之活性並無改變，且於蛋白激酶A的動力分析上(Vmax、S0.5) CLP組（實驗組）與對照組均無統計上的改變，故認為敗血症早期之血糖值的上升並非經由蛋白激酶A所調節，可能藉由他種蛋白激酶的影響。

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並列摘要

Sepsis-inducd glucose dyshomeostasis has been characterizated 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 kianase were cdompleted. 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 carbohyduate metabolism during early sepsis. The work was performed by suing an animal septic model, induced by cecal ligation and puncture (CLP) operation. Through the measurement of blood surgar, 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 cativities 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.

並列關鍵字

sepis ； protein kinase ； early stage

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早期敗血症時大白鼠肝中蛋白激酶A之動力探討

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