ArticleJournal of Crohn's & colitis2026
A metabolic constraint in de novo NAD+ synthesis drives mucosal inflammation in IBD.
Article in Journal of Crohn's & colitis, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Tracing NADCell reports · 2026Article
- Microbial metabolic memory in inflammatory bowel disease: microbiota-derived metabolites, host-microbe reprogramming, and relapse susceptibility.Frontiers in microbiology · 2026Review
- The aryl hydrocarbon receptor and kynurenine pathway: connecting inflammatory bowel disease and depression via the microbiota gut brain axis.Frontiers in neuroscience · 2026Review
- Gut microbiota-derived metabolites and IL-22 signaling in inflammatory bowel disease: context-dependent regulation of mucosal repair and inflammation.Frontiers in immunology · 2026Review
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Authors and funding
35 authors.
Funding
Abstract
backgroundInflammatory bowel disease (IBD) is associated with energy deficiency and perturbed metabolism of the essential amino acid tryptophan (Trp).
objectiveWe aimed to determine whether excessive Trp degradation fuels or compensates for inflammation through de novo nicotinamide adenine dinucleotide (NAD+) synthesis.
designA prospective systems medicine approach (metabolomics, transcriptomics) was employed longitudinally in patients with advanced IBD therapy. Findings were validated with targeted Trp metabolomics in experimental colitis and in vitro in fibroblasts, intestinal epithelial cells (IECs), and peripheral blood mononuclear cells (PBMCs).
resultsActive IBD is marked by enhanced Trp degradation driven by inflammatory cytokines through the JAK/STAT pathway. Trp catabolism results in accumulation of quinolinic acid (QA) and NAD + depletion due to reduced expression of QPRT, the enzyme converting QA to NAD+. QPRT knockdown enhances inflammation, while NAD + precursor supplementation (e.g. nicotinamide riboside [NR]) restores cellular energy and reduces inflammation in vitro and in dextran sodium sulfate (DSS)-induced colitis.
conclusionA metabolic bottleneck at QPRT prevents efficient NAD+ synthesis from Trp in IBD, sustaining inflammation. Restoring NAD + is a promising therapeutic strategy.
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