The hyper metabolic response during acute inflammation in sepsis is rapidly replaced by a hypo metabolic state as the organism struggles to balance severe stress responses of resistance and tolerance. Conceptually, therapeutic targeting of mitochondrial bioenergetic pathways may resolve immune and multi-organ failure and improve survival. Current pre-clinical data are consistent with the postulate that dysfunction of the mitochondrial pyruvate dehydrogenase complex drives many of the immune-metabolic complications of severe infection. Targeting this pathway resolves epigenetic, bioenergetic, nutritional, and oxidation/reduction dysregulation in cells and organs and provides survival benefit during the acute immune response.
Manal Zabalawi, Barbara K Yoza, Peter S Stacpoole* and Charles E McCall
Journal of Clinical Nutrition & Dietetics received 518 citations as per google scholar report