We hypothesized that decreased NAD+ in the intestinal epithelium during inflammation renders SIRT1 unable to activate PGC1α, resulting in decreased mitochondrial biogenesis and subsequent mitochondrial dysfunction...We also found a decrease in the intestional NAD+ levels in ulcerative colitis patients…Treatment of mice undergoing experimental colitis with an NAD+ precursor [nicotinamide riboside (NR), 500 mg/kg/day] decreased the severity of colitis, restored mitochondrial function, and increased active PGC1α levels...