Key Points
- To determine whether increased hepatic secretion of apolipoprotein B during Escherichia coli sepsis results from enhanced protein synthesis or diminished degradation.
- Induced sepsis in male Lewis rats (225–275 g) via intravenous injection of 3.8 x 10^8 live E. coli colonies per 100 g body weight.
- Isolated primary hepatocytes 24 hours post-injection and labeled them with 35S-methionine to assess apolipoprotein B secretion, synthesis, and pulse-chase degradation.
- Assessed cellular triglyceride mass, de novo triglyceride synthesis using 3H2O incorporation, and hepatic apolipoprotein B mRNA expression and editing.
- Hepatocytes from septic rats secreted twice as much apolipoprotein B-48 and total apolipoprotein B compared to controls.
- Sepsis increased cellular triglyceride mass by 86%, driven by stimulated triglyceride synthesis from newly formed fatty acids.
- Apolipoprotein B synthesis rates, mRNA levels, and mRNA editing remained unchanged, whereas the rate of apolipoprotein B degradation significantly decreased.
Structured PICO
Does E. coli sepsis increase hepatic apolipoprotein B secretion by inhibiting degradation in male Lewis rats?
PPopulationMale Lewis rats (225-275 g)
IInterventionIntravenous injection of 3.8 x 10(8) live E. coli colonies/100 g body weight to induce sepsis
OOutcomeHepatic secretion of apoB (apoB-48 and total apoB)surrogate
E. coli sepsis increases hepatic apolipoprotein B secretion by decreasing the degradation of newly synthesized apoB, contributing to hypertriglyceridemia.