Escherichia coli sepsis increases hepatic apolipoprotein B secretion by inhibiting degradation.
Escherichia coli sepsis increases hepatic apolipoprotein B secretion by inhibiting degradation.
复制标题
大肠杆菌败血症通过抑制降解来增加肝载脂蛋白 B 的分泌。
DOI：
10.1007/s11745-000-0622-y
复制
发表时间：
2000
期刊：
影响因子：
1.9
通讯作者：
Lanza-Jacoby,SP
中科院分区：
文献类型：
--
作者：
Phetteplace,HW;Sedkova,N;Hirano,KI;Davidson,NO;Lanza-Jacoby,SP
Sepsis leads to hypertriglyceridemia in both humans and animals. Previously, we reported that plasma very low density lipoprotein apolipoprotein (apo) B and hepatic production of apoB increased duringEscherichia colisepsis. The present experiments were undertaken to determine whether the altered hepatic secretion of apoB was associated with an increase in synthesis or a decrease in degradation rate. Sepsis was induced in male, Lewis rats (225–275 g) by intravenous injection of 3.8×108liveE. colicolonies/100 g body. Twenty‐four hours later rats were sacrificed, and primary hepatocytes were prepared and incubated overnight with35S‐methionine. Hepatocytes fromE. coli‐treated rats secreted twice as much apoB‐48 and total apoB than the hepatocytes from control rats.Escherichia colisepsis increased celular triglyceride mass by 86%, which was due to a stimulation in triglyceride synthesis from newly synthesized fatty acids, measured by3H2O incorporation into triglycerides. The apoB synthesis rate, apoB mRNA levels, and apoB mRNA editing were not altered duringE. colisepsis. The pulse‐chase experiments showed that the rate of apoB degradation decreased inE. coli‐treated rats. These findings demonstrate that the secretion of apoB is regulated posttranslationally duringE. colisepsis by decreasing the degradation of newly synthesized apoB, which contributes to the development of hypertriglyceridemia.
