Lipid metabolism in infection

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Abstract
Lipid metabolism is affected in a variety of ways during infection, depending on the causative agents. This interaction is further modulated by the nutritional status of the host and the severity of the infection. The most profound effects occur with gram-negative bacterial infections, endotoxemia, and sepsis. The duration and severity of infection, fever, and age represent important variables. The major lipid changes involve triglycerides, free fatty acids, and ketone bodies, the partially oxidized products of fatty acids by the liver. The changes in phospholipids and cholesterol appear to be trivial with respect to the survival mechanisms of the host. Elevated triglyceride concentrations during infection are primarily caused by impaired lipoprotein lipolytic activity. The level of free fatty acids is the result of the interplay of the antilipolytic action of insulin and the fat mobilization effect of catecholamines. Dietary manipulations, particularly in amounts of glucose, also alter the contribution of free fatty acids to the total energy requirements. Similarly, ketogenesis and thus ketone body levels are influenced by dietary manipulations, insulin level, and severity of infection. Lipid-dependent, protein-sparing therapies are most effective during states where starvation ketonemia exists. Substantial preservation of body cell mass may occur with the intake of protein intravenously or orally, at a concentration approaching 1.5 to 2 g of protein/kg of intitial body weight per day. Where fast-induced ketosis does not result from exclusion of exogenous carbohydrate, improved utilization of nitrogen may occur through the use of carbohydrate; however, the benefits of such therapy to visceral protein synthesis are yet to be determined.