Purpose of review Despite increasing evidence that critically ill patients have lower energy requirements than expected, most guidelines continue to recommend elevated caloric requirements in these patients, particularly in septic patients. This practice leads to liver dysfunction when artificial nutrition is employed and worsens the prognosis of these patients. This review is focused on recent developments in the pathogenesis of artificial nutrition associated liver dysfunction in critically ill patients.

Recent findings The liver plays a pivotal role in managing nutritional substrates, and it is involved in the inflammatory response to injury and sepsis. The landmark phenomenon is insulin resistance and changes in the metabolic fates of glucose and fat. Glucose and lipids can act as toxics synergistically with inflammation to induce liver dysfunction. There are experimental evidences that insulin resistance in critically ill patients can share the same biochemical mechanisms and metabolic fates involved in insulin resistance of type 2 diabetes mellitus and metabolic syndrome. Furthermore, steatosis is also a common feature in both clinical pictures

Summary The pathogenesis of artificial nutrition associated with liver dysfunction is related to overfeeding and sepsis with a pathophysiology, similar to metabolic syndrome and type 2 diabetes. Changing nutritional strategies and adding new drugs will prevent, in part, liver dysfunction in these patients.