Based on these observations on PUFA metabolism in clinical and experimental sepsis, several general statements can be made: (1) The metabolic response to injury and the metabolic processes of hypermetabolism and organ failure effect PUFA metabolism independent of starvation and of the presence or type of parenteral nutrition. (2) PUFA metabolism in sepsis is affected by starvation, the type of feeding used, and the fat composition of that feeding. The current fat formulations based in soy-bean oil can support some components of the plasma PUFA profile in hypermetabolism, but not in MOF. Adverse effects of the fat emulsion, however, may be occurring in settings of sepsis. These effects are related to alterations in mortality and in white blood cell and mononuclear cell function and are in the early stages of investigation. (3) Multiple organ failure may be associated with alterations in desaturation and elongation capacity consistent with the hepatic insufficiency that is occurring in this setting. (4) Experimental studies indicate the potential to modulate cell-cell communication with alterations in dietary PUFA composition. The potential for developing therapeutic tools for use in sepsis and HOF seems to be present. Continued research and communication is necessary for them to come to fruition.