Alston-Smith J, Ljungqvist O, Boija P O, Ware J, Ekdahl K N
Department of Clinical Immunology and Transfusion Medicine, University Hospital, Uppsala, Sweden.
Acta Chir Scand. 1990 Oct;156(10):677-81.
Altered glucose metabolism is one of the commonly observed sequelae of sepsis and septic shock. The present investigation was undertaken to determine the role of endotoxin (ET) upon hepatocyte glucoregulation, by measuring the activity of pyruvate kinase (PK), a key glycolytic enzyme. Hepatocytes were exposed to endotoxin concentrations known to occur in vivo during sepsis, i.e., from 1 X 10(-14) to 1 X 10(-8) g/ml. The alteration of the enzyme activities after addition of epinephrine, glucagon, insulin and calcium ionophore A23187 with and without ET preincubation were also examined. ET alone decreased the PK activity by 12% at all concentrations tested. The basal inhibition of the enzyme caused by epinephrine (-48%) was partially blocked by ET preincubation above 1 X 10(-10) g/ml. There were no ET-(glucagon, calcium ionophore, insulin) interaction. These in vitro results do not support pyruvate kinase as a site of hepatic enzyme regulation defect in endotoxaemia.
葡萄糖代谢改变是脓毒症和脓毒性休克常见的后遗症之一。本研究旨在通过测量关键糖酵解酶丙酮酸激酶（PK）的活性，确定内毒素（ET）对肝细胞葡萄糖调节的作用。将肝细胞暴露于脓毒症期间体内已知会出现的内毒素浓度下，即1×10⁻¹⁴至1×10⁻⁸ g/ml。还检测了在有和没有ET预孵育的情况下，加入肾上腺素、胰高血糖素、胰岛素和钙离子载体A23187后酶活性的变化。在所有测试浓度下，单独的ET均使PK活性降低了12%。肾上腺素引起的该酶基础抑制（-48%）在高于1×10⁻¹⁰ g/ml的ET预孵育时被部分阻断。不存在ET - （胰高血糖素、钙离子载体、胰岛素）相互作用。这些体外实验结果不支持丙酮酸激酶是内毒素血症中肝脏酶调节缺陷的位点。
