We have previously shown that mitochondrial dysfunction and disruption of mitochondrial biogenesis contribute to the pathogenesis of IBD. Peroxisome Proliferator-activated Receptor–gamma Coactivator 1-alpha (PGC1α) is the primary regulator of mitochondrial biogenesis. In patients with ulcerative colitis (UC) and mice undergoing experimental colitis, the transcript and protein levels of PGC1α are reduced, which is concomitant with a decrease in mitochondrial function, derangement of mitochondrial structure, and an increase in oxidative stress.