**7. Conclusion**

During the septic response, altered VLDL metabolism is responsible for the lipemia of sepsis. Entotoxin promoted changes are biphasic. In the early stage hypertriglyceridemia is accompanied by increased circulating fatty acids levels and a rise in large TG-rich VLDL, whereas the later stage is characterized by high levels of hepatic apoB transcript and TG-

poor VLDL accumulation. In the later stage, the endotoxin induced VLDL secretion is more accentuated in periportal cells. Kupffer cells released products directly promote VLDL assembly and secretion and increase apoB mRNA levels, among these products the cytokines TNF–α, IL-6 and IL-1β and other mediator/s could play a role in the enhancement of VLD secretion.
