Mechanism of inflammation-triggered glycaemic control

Strong suppression of de novo glucose production by the liver, e.g. gluconeogenesis, during acute inflammation is one of the major characteristics of the aberrant metabolic state and reason of death in septic patients. Interference with hormone signalling and the subsequent suppression of a key gluconeogenic enzyme, phosphoenolpyruvate carboxykinase (PEPCK), through pro-inflammatory mediators importantly contribute to the hypoglycaemic phenotype in sepsis. However, the molecular mechanisms of aberrant PEPCK gene regulation under these conditions remain unknown. In present study we aimed to elucidate in vivo dysf…