Lipids and the critically ill patient.

Abstract

Lipid metabolism is altered in the critically ill patient as a result of changes in the status of hormones and other mediators [for reviews see, 1–3]. Enhanced mobilization of adipose tissue triacylglycerol stores is characteristic of the metabolic response to severe stress. This process is promoted by catecholamines and inflammatory cytokines, such as tumor necrosis factor (TNF)and interleukin (IL)-1, and is exaggerated by the decreased insulin sensitivity of adipose tissue. The release of fatty acids from adipose tissue is frequently in excess of energy requirements. Those fatty acids not oxidized may be re-esterified into triacylglycerols in the liver and packaged into very low-density lipoproteins (VLDLs). Hepatic triacylglycerol production is increased in critical illness and this can lead to lipid deposition (steatosis) in the liver. Nevertheless, hepatic triacylglycerol output (as VLDLs) is also increased in critical illness. In some conditions (e.g. trauma or after surgery) triacylglycerol clearance is not impaired (or may even be increased) and so plasma triacylglycerol concentrations remain normal (or may even be decreased). However, in some conditions (e.g. sepsis), the activity of adipose tissue lipoprotein lipase is suppressed by inflammatory cytokines (e.g. TNF and IL-1) and insulin resistance, and so triacylglycerols are not efficiently cleared from the circulation. Thus, hypertriacylglycerolemia occurs in such patients. VLDLs can bind endotoxin and target it for degradation in liver parenchymal cells. Thus, the increase in VLDL concentration may be, in part, a protective mechanism. The plasma cholesterol concentration is decreased in stress conditions, with the concentrations of both low(LDLs) and highdensity lipoproteins (HDLs) being decreased. This decrease occurs despite increased hepatic cholesterol production. The decreased HDL concentration