Stress hyperglycaemia, first described by Claude Bernard in 1878, occurs when an acute stressor such as sepsis and other acute illness causes increased release of glucagon, cortisol, catecholamines, growth hormone, and pro-inflammatory cytokines that promote hepatic gluconeogenesis, glycogenolysis, inhibition of peripheral glucose uptake, and inhibition of insulin release [11],[12]. Here, GH1 is linked to Sepsis.