The metabolic response to burn injury is highly complex and remains a subject of intensive multidisciplinary research. The precise mechanisms underlying the profound metabolic, hormonal, and inflammatory disturbances associated with severe burns are not yet fully understood. Following a burn injury, the body’s ability to maintain homeostasis is rapidly and systemically impaired, resulting in the development of a pathological state known as burn disease. Modern clinical and experimental studies have demonstrated that, in addition to localized skin damage and disruption of histohematic barriers, burns, especially those involving more than 20% of the total body surface area, trigger a generalized cascade of immune and inflammatory reactions known as the systemic inflammatory response syndrome. Simultaneously, a profound metabolic shift occurs, characterized by a persistent hypermetabolic and hypercatabolic state. This hypermetabolic response is accompanied by intensive proteolysis and catabolism of skeletal muscle proteins to provide substrates for gluconeogenesis, uncontrolled lipolysis of adipose tissue with the release of free fatty acids, and a significant surge in energy expenditure. Ultimately, these alterations contribute to the development of multiple organ dysfunction syndrome.