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NAD+ precursors and intestinal inflammation: therapeutic insights involving gut microbiota

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dc.contributor.authorNiño-Narvión, Julia
dc.contributor.authorRojo-López, Marina Idalia
dc.contributor.authorMartinez-Santos, Patricia
dc.contributor.authorRossell, Joana
dc.contributor.authorRuiz Alcaraz, Antonio José
dc.contributor.authorAlonso, Núria
dc.contributor.authorRamos-Molina, Bruno
dc.contributor.authorMauricio, Didac
dc.contributor.authorJulve, Josep
dc.contributor.departmentBioquímica y Biología Molecular B e Inmunología
dc.contributor.otherFacultad de Biología
dc.date.accessioned2026-01-13T12:03:52Z
dc.date.available2026-01-13T12:03:52Z
dc.date.copyright© 2023 by the authors
dc.date.issued2023-06-30
dc.description.abstractThe oxidized form of nicotinamide adenine dinucleotide (NAD+) is a critical metabolite for living cells. NAD+ may act either as a cofactor for many cellular reactions as well as a coenzyme for different NAD+-consuming enzymes involved in the physiological homeostasis of different organs and systems. In mammals, NAD+ is synthesized from either tryptophan or other vitamin B3 intermediates that act as NAD+ precursors. Recent research suggests that NAD+ precursors play a crucial role in maintaining the integrity of the gut barrier. Indeed, its deficiency has been associated with enhanced gut inflammation and leakage, and dysbiosis. Conversely, NAD+-increasing therapies may confer protection against intestinal inflammation in experimental conditions and human patients, with accumulating evidence indicating that such favorable effects could be, at least in part, mediated by concomitant changes in the composition of intestinal microbiota. However, the mechanisms by which NAD+-based treatments affect the microbiota are still poorly understood. In this context, we have focused specifically on the impact of NAD+ deficiency on intestinal inflammation and dysbiosis in animal and human models. We have further explored the relationship between NAD+ and improved host intestinal metabolism and immunity and the composition of microbiota in vivo. Overall, this comprehensive review aims to provide a new perspective on the effect of NAD+-increasing strategies on host intestinal physiology.
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dc.format.extent24
dc.identifier.citationNutrients 2023, 15(13), 2992
dc.identifier.doihttps://doi.org/10.3390/nu15132992
dc.identifier.eissn2072-6643
dc.identifier.urihttp://hdl.handle.net/10201/186289
dc.languageeng
dc.publisherMDPI
dc.relationThis work was funded by the Ministerio de Sanidad y Consumo, Instituto de Salud Carlos III (Madrid, Spain) grant PI21/00770 (to J.J.) and PI21/00817 (to N.A.), FEDER “Una manera de hacer Europa”. B.R-M was supported by the “Miguel Servet Type I” program (CP19/00098, ISCIII, Spain; co-funded by the Fondo Europeo de Desarrollo Regional-FEDER). M. I. R-L holds a predoctoral grant SLT017/20/000107 from Pla Estratègic de Recerca i Innovació en Salut (PERIS) 2021–2024 of Generalitat de Catalunya. This work was supported by CIBER-Consorcio Centro de Investigación Biomédica en Red-CIBERDEM (leading group CB15/00071, D.M., and CB07/08/0016), Instituto de Salud Carlos III, Ministerio de Ciencia e Innovación. Institut de Recerca de l’Hospital de la Santa Creu i Sant Pau is accredited by the Generalitat de Catalunya as Centre de Recerca de Catalunya (CERCA).
dc.relation.publisherversionhttps://www.mdpi.com/2072-6643/15/13/2992
dc.rightsAttribution 4.0 International*
dc.rights.accessRightsinfo:eu-repo/semantics/openAccess
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subjectNiacin
dc.subjectAging
dc.subjectNicotinamide
dc.subjectMetabolomics
dc.subjectBiomarker
dc.subjectTherapy
dc.subjectIntestinal bowel disease
dc.subjectColitis
dc.subjectPellagra
dc.subjectDiabetes mellitus
dc.subject.odsNo relacionado con ningún objetivo de desarrollo sostenible
dc.titleNAD+ precursors and intestinal inflammation: therapeutic insights involving gut microbiota
dc.typeinfo:eu-repo/semantics/article
dc.type.versioninfo:eu-repo/semantics/publishedVersion
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relation.isAuthorOfPublicationc5d54ef3-bd3b-4330-b4a1-252ab278925b
relation.isAuthorOfPublication.latestForDiscoveryc5d54ef3-bd3b-4330-b4a1-252ab278925b
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