脓毒症大鼠体内肝脏胆固醇生成和脂肪酸合成速率增加：胰岛素可能参与其中的证据。

Increased rates of hepatic cholesterogenesis and fatty acid synthesis in septic rats in vivo: evidence for the possible involvement of insulin.

de Vasconcelos P R, Kettlewell M G, Gibbons G F, Williamson D H

Nuffield Department of Clinical Medicine, Radcliffe Infirmary, Oxford, U.K.

Clin Sci (Lond). 1989 Feb;76(2):205-11. doi: 10.1042/cs0760205.

Abstract

Sepsis induced by caecal ligation and puncture increased the rates of hepatic cholesterogenesis and fatty acid synthesis in vivo compared with sham-operated rats. These changes were accompanied by higher concentrations of lactate and pyruvate in blood and liver and an increase in plasma insulin. 2. The total activity of hydroxymethylglutaryl-coenzyme A (HMG-CoA) reductase (EC 1.1.1.88) in liver was increased by sepsis, but there was no significant change in the expressed activity. Short-term insulin deficiency (induced by mannoheptulose or streptozotocin) decreased the rates of cholesterogenesis and fatty acid synthesis in livers of septic rats but did not alter the expressed/total activity of HMG-CoA reductase. 3. It is concluded that the increased rate of hepatic cholesterogenesis in septic rats is in part a result of the higher plasma insulin, the hormone acting to maintain the total activity of HMG-CoA reductase and to stimulate a step before the formation of HMG-CoA. 4. These changes may contribute to the hypertriacylglycerolaemia associated with sepsis.

摘要

与假手术组大鼠相比，盲肠结扎穿孔诱导的脓毒症增加了体内肝脏胆固醇生成和脂肪酸合成的速率。这些变化伴随着血液和肝脏中乳酸和丙酮酸浓度的升高以及血浆胰岛素水平的增加。2. 脓毒症使肝脏中羟甲基戊二酰辅酶A（HMG-CoA）还原酶（EC 1.1.1.88）的总活性增加，但表达活性无显著变化。短期胰岛素缺乏（由甘露庚酮糖或链脲佐菌素诱导）降低了脓毒症大鼠肝脏中胆固醇生成和脂肪酸合成的速率，但未改变HMG-CoA还原酶的表达/总活性。3. 得出的结论是，脓毒症大鼠肝脏胆固醇生成速率增加部分是由于血浆胰岛素水平升高，该激素作用于维持HMG-CoA还原酶的总活性并刺激HMG-CoA形成之前的一个步骤。4. 这些变化可能导致与脓毒症相关的高甘油三酯血症。