In Crohn's disease and ulcerative colitis, inflammation blocks its own healing

What To Know

Researchers from Kiel University and U.S. collaborators report that chronic intestinal inflammation reduces production of the enzyme QPRT, causing a bottleneck in NAD+ synthesis from tryptophan so the intestinal lining faces an energy shortfall.

Independent patient cohorts and experimental models were used, and follow-up studies showed metabolic compensation through alternative NAD+ precursors—particularly nicotinamide—and preliminary links to the gut microbiome.

The studies together provide a mechanistic rationale for investigating nicotinamide (a form of vitamin B3) as a therapy that can bypass the blocked step; the article cites the ongoing ORNATUS clinical trial testing locally delivered nicotinamide in ulcerative colitis.

These findings shift attention to cellular metabolism—NAD+ synthesis and its regulation—alongside immune pathways and the microbiome as contributors to persistent inflammation in IBD.

They do not report patient-level treatment results here, but identify potential therapeutic targets and explain why trials of NAD+-boosting approaches are biologically plausible. Curator's note grounded in the Medical Xpress article and linked publications; Cure8 has not reviewed the primary papers beyond the source text.