Severe burn causes a catabolic response with profound effects on glucose and muscle protein metabolism. This response is characterized by hyperglycemia and loss of muscle mass, both of which have been associated with significantly increased morbidity and mortality. In critically ill surgical patients, obtaining tight glycemic control with intensive insulin therapy was shown to reduce morbidity and mortality and has increasingly become the standard of care. In addition to its well-known anti-hyperglycemic action and reduction in infections, insulin promotes muscle anabolism and regulates the systemic inflammatory response. Despite a demonstrated benefit of insulin administration on the maintenance of skeletal muscle mass, it is unknown if this effect translates to improved clinical outcomes in the thermally injured. Further, insulin therapy has the potential to cause hypoglycemia and requires frequent monitoring of blood glucose levels. A better understanding of the clinical benefit associated with tight glycemic control in the burned patient, as well as newer strategies to achieve and maintain that control, may provide improved methods to reduce the clinical morbidity and mortality in the thermally injured patient.