31fcffc864a51239c3790df6c5d30578 301308.pdf 60b38a73f9a510455c9dd828e3873bd20bef6782 301308.pdf dee283f05dfd1d8a006a16735e8588f6a4b7573c451aca3efe6dc6411cc1a665 301308.pdf Title: NAD+ Precursors and Intestinal Inflammation: Therapeutic Insights Involving Gut Microbiota Subject: The 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. Keywords: diabetes mellitus; niacin; aging; nicotinamide; metabolomics; biomarker; therapy;intestinal bowel disease; colitis; pellagra Author: Julia Niño-Narvión, Marina Idalia Rojo-López, Patricia Martinez-Santos, Joana Rossell, Antonio J. Ruiz-Alcaraz, Núria Alonso, Bruno Ramos-Molina, Didac Mauricio and Josep Julve Creator: LaTeX with hyperref Producer: pdfTeX-1.40.21 CreationDate: Mon Jul 3 06:30:29 2023 CEST ModDate: Mon Jul 3 06:56:11 2023 CEST Custom Metadata: no Metadata Stream: no Tagged: no UserProperties: no Suspects: no Form: none JavaScript: no Pages: 24 Encrypted: no Page size: 595.276 x 841.89 pts (A4) Page rot: 0 File size: 1241479 bytes Optimized: no PDF version: 1.7 name type encoding emb sub uni object ID ------------------------------------ ----------------- ---------------- --- --- --- --------- URXFAW+VnURWPalladioL Type 1 Custom yes yes no 10 0 FORXJC+URWPalladioL-Bold Type 1 Custom yes yes no 15 0 BWBQOZ+URWPalladioL-Roma Type 1 Custom yes yes no 20 0 KQWRVY+URWPalladioL-Ital Type 1 Custom yes yes no 24 0 WYFLDJ+VnURWPalladioL-Bold Type 1 Custom yes yes no 28 0 HGMNRX+TimesNewRomanPS-BoldItalicMT Type 1C WinAnsi yes yes no 46 0 FBEGNP+PalatinoLinotype,Bold TrueType WinAnsi yes yes no 75 0 FBEGOA+PalatinoLinotype CID TrueType Identity-H yes yes yes 78 0 FBEGOB+PalatinoLinotype TrueType WinAnsi yes yes no 84 0 FBEGOD+PalatinoLinotype,Italic TrueType WinAnsi yes yes no 87 0 FBEHJB+PalatinoLinotype TrueType MacRoman yes yes no 90 0 FBEGNP+PalatinoLinotype,Bold TrueType WinAnsi yes yes no 125 0 FBEGOA+PalatinoLinotype CID TrueType Identity-H yes yes yes 128 0 FBEGOB+PalatinoLinotype TrueType WinAnsi yes yes no 134 0 FBEGOD+PalatinoLinotype,Italic TrueType WinAnsi yes yes no 137 0 FBEHJB+PalatinoLinotype TrueType MacRoman yes yes no 140 0 ERPOGD+PazoMath-Italic Type 1 Builtin yes yes no 148 0 VVSYYB+EURM10 Type 1 Builtin yes yes no 156 0 NJAOJC+CMSY10 Type 1 Builtin yes yes no 160 0 Jhove (Rel. 1.28.0, 2023-05-18) Date: 2024-10-12 02:43:41 CEST RepresentationInformation: 301308.pdf ReportingModule: PDF-hul, Rel. 1.12.4 (2023-03-16) LastModified: 2024-10-11 10:13:06 CEST Size: 1241479 Format: PDF Version: 1.7 Status: Well-Formed and valid SignatureMatches: PDF-hul MIMEtype: application/pdf PDFMetadata: Objects: 703 FreeObjects: 1 IncrementalUpdates: 0 DocumentCatalog: PageLayout: SinglePage PageMode: UseNone Outlines: Item: Title: Background Destination: section.1 Item: Title: Intestinal Inflammation and Dysbiosis in NAD+-Deficient States Destination: section.2 Children: Item: Title: Modifiable Factors Destination: subsection.2.1 Children: Item: Title: Pellagra, as an Example of Nutritional Deficiency Destination: subsubsection.2.1.1 Item: Title: Chronic Alcoholism Destination: subsubsection.2.1.2 Item: Title: Chemotherapy Destination: subsubsection.2.1.3 Item: Title: Non-Modifiable Factors Destination: subsection.2.2 Children: Item: Title: Aging Destination: subsubsection.2.2.1 Item: Title: Sex Destination: subsubsection.2.2.2 Item: Title: Immunomodulatory Conditions Destination: subsubsection.2.2.3 Item: Title: Metabolic-Related Conditions Destination: subsubsection.2.2.4 Item: Title: Linking Intestinal and Neurological Conditions: Autism Spectrum Disorder Destination: subsubsection.2.2.5 Item: Title: NAD+-Increasing Therapies in the Treatment of Intestinal Inflammation Destination: section.3 Children: Item: Title: Nicotinic Acid (NA) Destination: subsection.3.1 Item: Title: Nicotinamide (NAM) Destination: subsection.3.2 Item: Title: Nicotinamide Mononucleotide (NMN) Destination: subsection.3.3 Item: Title: Nicotinamide Riboside (NR) Destination: subsection.3.4 Item: Title: Conclusions and Perspectives Destination: section.4 Item: Title: References Destination: section.4 Info: Title: NAD+ Precursors and Intestinal Inflammation: Therapeutic Insights Involving Gut Microbiota Author: Julia Niño-Narvión, Marina Idalia Rojo-López, Patricia Martinez-Santos, Joana Rossell, Antonio J. Ruiz-Alcaraz, Núria Alonso, Bruno Ramos-Molina, Didac Mauricio and Josep Julve Subject: The 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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