IL1B and Hyperglycemia: It appears that hormones like catecholamines and inflammatory cytokines such as TNFα and IL-1β attenuate or “blunt” pancreatic insulin secretion, so the β cells of the pancreas produce less insulin than needed due to the cellular energy depletion specific to severe burns [128]; this phenomenon might be explained by the “damage” to β cells produced by stress hormones and/or inflammatory cytokines [129] or by alteration of GLUT2 expression in β cells induced by hyperglycemia and increased FFA levels [129,130], which are common traits in the hypermetabolic state of severely burned patients.