biostudies-arrayexpressMarie RumplerMus musculushttps://www.ebi.ac.uk/biostudies/studies/E-MTAB-14177NAD+ is a crucial cofactor for the activity of various enzymes, including sirtuins and ADP-ribosyl transferases, and its decline is associated with aging and metabolic-related diseases. Therefore, a strong interest has been raised in the therapeutic use of NAD+ precursors (Vitamin B3s), but many suffer from poor bioavailability and adverse effects. This study characterizes the metabolic impact of dihydronicotinamide riboside, a recently identified novel form of NAD+ precursor. Upon oral administration in mice, NRH reaches all tissues examined. Chronic administration in low-fat diet-fed mice showed negligible metabolic effects, while high-fat diet-fed mice were protected against body weight gain and glucose intolerance. However, our study also unveiled potential side effects at higher doses. Thus, NRH could constitute an alternative NAD+ boosting strategy to prevent diet-induced metabolic complications and conditions associated with low NAD+ levels, but the therapeutic window must be optimized to maximize benefits and minimize risks.biostudies-arrayexpressNucleic Acid Extraction - DNA from mouse feces samples were obtained using a Quick-DNA Fecal/Soil Microbe Miniprep Kit from Zymo (#D6010).Library Construction - Libraries were generated using a \\"16S library prep with ZYMO Quick-16S_Plus\\" library prep kit according to manufacturers’ instructions. Libraries have been pooled prior to sequencing and quantified by a qubit DNA High Sensitivity assay (Thermo, #Q32851).Sequencing - The pooled library was sequencing on an Illumina MiSeq using 300 PE sequencing chemistry.Sample Collection - Male and Female C57Bl/6NTac were purchased from Taconic. All mice were kept in a standard temperature- and humidity-controlled environment with a 12h:12h light-dark cycle. Mice had nesting material and ad libitum access to water and commercial diets. For the control diet (chow), mice were fed a regular mouse housing diet (Safe®150).OrganizationMINSEQE ScoreAssays and DataProcessed DataMAGE-TAB FilesData Transformation - Data preprocessing was done using DADA2 (Callahan, Nature Methods, 2016). Downstream analysis was performed using Phyloseq (McMurdie, Plos One, 2013).Sequence Alignment - Data preprocessing was done using DADA2 (Callahan, Nature Methods, 2016).MetabolomicsUnknownTranscriptomicsGenomicsProteomicsIllumina MiSeqDNA-seqMus musculusMarie RumplerJulie RusseilSofia MocoCarles CantoBart DeplanckeFaisal HayatStefan ChristenVincent GardeuxHoria HashimiClémence SteinerJudith Giroud-GerbetantMaria Pilar GinerRiekelt HoutkooperKasper VintenMagali JoffraudJose Luis Sanchez GarciaMarie MigaudGuido Van MierloLaurine Van GijnfalseMetabolic effects of chronic dihydronicotinamide riboside (NRH) administration in mice - Microbiome 16S rRNA sequencing of murine feces (NRH treatment)NAD+ is a crucial cofactor for the activity of various enzymes, including sirtuins and ADP-ribosyl transferases, and its decline is associated with aging and metabolic-related diseases. Therefore, a strong interest has been raised in the therapeutic use of NAD+ precursors (Vitamin B3s), but many suffer from poor bioavailability and adverse effects. This study characterizes the metabolic impact of dihydronicotinamide riboside, a recently identified novel form of NAD+ precursor. Upon oral administration in mice, NRH reaches all tissues examined. Chronic administration in low-fat diet-fed mice showed negligible metabolic effects, while high-fat diet-fed mice were protected against body weight gain and glucose intolerance. However, our study also unveiled potential side effects at higher doses. Thus, NRH could constitute an alternative NAD+ boosting strategy to prevent diet-induced metabolic complications and conditions associated with low NAD+ levels, but the therapeutic window must be optimized to maximize benefits and minimize risks.2026-03-09T00:00:00Z2026-03-09T02:02:49.789Z2024-06-13T09:22:09.365ZE-MTAB-14177ERP161083EFO_0002944EFO_0004170EFO_0002693EFO_0004917EFO_0005518EFO_0003816EFO_0004184