In trauma/sepsis, lipolysis is stimulated by the release of stress hormones, catecholamines, and inflammatory mediators. Post-trauma, patients have increased lipolysis and utilize these adipose deposits as a primary fuel source. With that said, lipid oxidation is also increased post-trauma. Following trauma, adipose tissue lipoprotein lipase is decreased, while muscle lipoprotein lipase activity is increased. However, following sepsis, muscle lipoprotein lipase activity is decreased. The metabolic response to stress involves most metabolic pathways within the body, accelerated metabolism of lean body mass, negative nitrogen balance, and muscle wasting. In the hypermetabolic state, stress causes an acceleration in overall energy expenditure, glucose production, as well as glucose cycling in liver and muscle. To support hypermetabolism and increased gluconeogenesis, fat is mobilized from adipose stores to provide energy. This occurs as the result of elevated levels of catecholamines as well as a decrease in insulin production. With that said, hypermetabolism may occur in patients who have experienced trauma or sepsis as caused by a cycle in which an increased rate of reesterification within adipose tissues takes place. To add, the increase in lipolysis also increases the amount of available glycerol for gluconeogenesis. During critical illness, circulating glycerol levels indicate increased whole body lipolysis and adipose tissue increases the storage of lipids. With this, the source of these released lipids is not yet known. However, the source of released lipids remains to be fully understood. In addition, adipose tissue increases storage of lipids during critical illness. With this, increased LPL and low-normal levels of HSL are present. In patients