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首页> 外文期刊>Shock: Molecular, cellular, and systemic pathobiological aspects and therapeutic approaches = The official journal of the Shock Society, the European Shock Society, the Brazilian Shock Society, the International Federation of Shock Societies >Liver protein kinase A activity is decreased during the late hypoglycemic phase of sepsis.
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Liver protein kinase A activity is decreased during the late hypoglycemic phase of sepsis.

机译：肝脏蛋白激酶活性却降低了在脓毒症的血糖过低的后期阶段。

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Changes in protein kinase A (PKA, or cAMP-dependent protein kinase) activity in the rat liver during different metabolic phases of sepsis were investigated. Sepsis was induced by cecal ligation and puncture (CLP). Experiments were divided into 3 groups: control, early sepsis, and late sepsis. Early and late sepsis refer to those animals killed at 9 and 18 h, respectively, after CLP. Hepatic PKA was extracted and partially purified by acid precipitation, ammonium sulfate fractionation, and diethylaminoethyl (DEAE)-cellulose chromatography. PKA was eluted from DEAE-cellulose column with a linear NaCl gradient. Two peaks of PKA, type I (eluted at low ionic strength) and type II (eluted at high ionic strength), were collected and their activities were determined on the basis of the rate of incorporation of [gamma-32-P]ATP into histone. The results show that during early sepsis, both type I and type II PKA activities remained unchanged. During late sepsis, type I PKA activity was decreased by 40.7-53.6%, whereas type II PKA activity was unaffected. Kinetic analysis of the data on type I PKA during the late phase of sepsis reveals that the Vmax (maximal velocity) values for ATP, cAMP, and histone were decreased by 40.7, 53.6, and 47.3%, respectively whereas the Km (substrate concentration required for half-maximal enzymatic activity) values for ATP, cAMP, and histone were unaltered. These data indicate that type I PKA was inactivated during the late hypoglycemic phase of sepsis in the rat liver. Because PKA-mediated phosphorylation plays an important role in the regulation of hepatic glucose metabolism, an inactivation of PKA may contribute to the development of hypoglycemia during the late phase of sepsis.
机译：蛋白激酶A (PKA,或变化cAMP-dependent蛋白激酶)的活动大鼠肝脏在不同代谢阶段脓毒症。盲肠的结扎和穿刺(CLP)。被分成3组:控制、早脓毒症和脓毒症晚期。是指动物死亡和18 h, 9点CLP后分别。提取并部分由酸纯化降水、硫酸铵分级,和diethylaminoethyl DEAE纤维素色谱法。deae纤维素柱与一个线性氯化钠梯度。在高离子强度)和II型(筛选了离子强度),收集和他们的活动的基础上确定的速度吗将[gamma-32-P] ATP组蛋白。结果表明,在早期败血症,I型和II型PKA活动依然存在不变。活动减少了-53.6%至40.7,而II型PKA活性不受影响。分析数据的I型PKA期间脓毒症显示Vmax的后期阶段(最大速度)值ATP,营地,和组蛋白下降了40.7、53.6和47.3%,分别而公里(衬底half-maximal酶所需浓度ATP的活动)值、营地和组蛋白没有改变。是灭活的血糖过低的末阶段的脓毒症大鼠肝脏。PKA-mediated磷酸化中扮演一个重要的在肝脏葡萄糖的调节作用新陈代谢,PKA可能造成的失活低血糖症的发展中脓毒症的后期阶段。

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