New York: Enhanced levels of a protein that induces the creation of fatty acid can lead to sepsis, a leading cause of death for patients in intensive care units, new research has found.
The UCP2 protein is enhanced in patients with sepsis, the findings showed.
"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.