A new research found that UCP2, an enhanced level of a protein, induces the creation of fatty acid can lead to sepsis. Sepsis is a leading cause of death for patients in intensive care units.
The most common cause of death in patients with sepsis is deterioration of the function of multiple organs. This syndrome has been called the multiple organ dysfunction syndrome (MODS). The organs most commonly affected are the lungs, liver, and kidneys.
The findings showed that UCP2 protein is enhanced in patients with sepsis. Meanwhile, insulin resistance and hyperglycaemia are common in severe sepsis.
“These results identify UCP2 as a potential therapeutic target in inflammatory diseases such as sepsis,” said Augustine Choi from Weill Cornell Medical College, New York.
The excessive systemic inflammation in individuals with sepsis damages organs and can lead to death.
Therapeutic options for sepsis are limited and the factors that promote this excessive response to infection are poorly understood. In mouse model of sepsis, lack of this protein ( UCP2) improved survival.
The authors determined that expression of UCP2 induces fatty acid synthesis, which in turn activates inflammatory pathways.
Given the roles of UCP2 in metabolic changes triggered by the immune response, further investigation of UCP2 in the context of cellular metabolism may be useful for elucidating mechanisms of human diseases, the researchers noted.
The study appeared in the Journal of Clinical Investigation.