The NAD+ Precursor Nicotinamide Riboside Enhances Oxidative Metabolism and Protects against High-Fat Diet-Induced Obesity
Open accessAbstract
As NAD(+) is a rate-limiting cosubstrate for the sirtuin enzymes, its modulation is emerging as a valuable tool to regulate sirtuin function and, consequently, oxidative metabolism. In line with this premise, decreased activity of PARP-1 or CD38-both NAD(+) consumers-increases NAD(+) bioavailability, resulting in SIRT1 activation and protection against metabolic disease. Here we evaluated whether similar effects could be achieved by increasing the supply of nicotinamide riboside (NR), a recently described natural NAD(+) precursor with the ability to increase NAD(+) levels, Sir2-dependent gene silencing, and replicative life span in yeast. We show that NR supplementation in mammalian cells and mouse tissues increases NAD(+) levels and activates SIRT1 and SIRT3, culminating in enhanced oxidative metabolism and protection against high-fat diet-induced metabolic abnormalities. Consequently, our results indicate that the natural vitamin NR could be used as a nutritional supplement to ameliorate metabolic and age-related disorders characterized by defective mitochondrial function.
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NR prevents and improves metabolic disorders such as high-fat diet-induced obesity and non-alcoholic fatty liver disease.
“Additionally, NR has been shown to prevent and improve metabolic disorders such as high-fat diet- induced obesity and non-alcoholic fatty liver disease (NAFLD).”
From NAD+ Precursors Nicotinamide Mononucleotide (NMN) and Nicotinamide Riboside (NR): Potential Dietary Contribution to Health (2023) · cites this paper as [95]
In Results, under “NR supplementation enhances energy expenditure” (page unavailable), NR significantly attenuated high-fat-diet-induced weight gain in mice, and their livers contained 40% less triglyceride. The paper does not establish that NR prevents or improves diagnosed NAFLD, nor does this prevention study show improvement of an existing disorder. (LLM, conf=0.86)
Experimental — accuracy not yet measuredNR supplementation (400 mg/kg/day) in mice increased NAD+ levels in liver and muscle, stimulated SIRT1 and SIRT3 activity, and enhanced mitochondrial function, oxidative metabolism, energy expenditure, and endurance performance.
“By increasing NAD+ levels in mice’s liver and muscle, NR supplementation (400 mg/kg/day) stimulated SIRT1 and SIRT3 activity, enhancing the mitochondrial function, oxidative metabolism, energy expenditure, and endurance performance [95].”
From NAD+ Precursors Nicotinamide Mononucleotide (NMN) and Nicotinamide Riboside (NR): Potential Dietary Contribution to Health (2023) · cites this paper as [95]
The Results sections report that 400 mg/kg/day NR increased liver and muscle NAD+, increased readouts of SIRT1 and SIRT3 activity, and improved measures of mitochondrial function and oxidative metabolism (page numbers unavailable). The energy-expenditure and endurance Results qualify the performance findings: both showed a tendency on chow but a significant improvement on a high-fat diet. The sentence omits that condition and presents sirtuin activity as the established cause of all the outcomes, whereas the Discussion notes that other NR actions may contribute. (LLM, conf=0.86)
Experimental — accuracy not yet measuredNR promoted metabolic flexibility by enhancing energy expenditure, attenuating high-fat diet-induced body weight gain and decreasing fat mass, with liver triglyceride levels decreasing by 40%.
“It promoted metabolic flexibility by enhancing energy expenditure, leading to a significant attenuation of high-fat diet-induced body weight gain and a decrease in fat mass, particularly in the liver, where triglyceride levels decreased by 40% [95].”
From NAD+ Precursors Nicotinamide Mononucleotide (NMN) and Nicotinamide Riboside (NR): Potential Dietary Contribution to Health (2023) · cites this paper as [95]
NR protected against detrimental metabolic effects of a high-fat diet including hyperinsulinemia, elevated total and LDL cholesterol, and weight gain, but had no effect on body weight when given with a normal chow diet.
“In addition, NR protected against the detrimental metabolic effects of a high-fat diet, including hyperinsulinemia, elevated levels of total and LDL cholesterol, and weight gain, although it had no effect on body weight when given with a normal chow diet [95].”
From NAD+ Precursors Nicotinamide Mononucleotide (NMN) and Nicotinamide Riboside (NR): Potential Dietary Contribution to Health (2023) · cites this paper as [95]
Higher NAD+ levels promote the deacetylase and deacylase activity of nuclear SIRT1 and mitochondrial SIRT3, which regulate mitochondrial function and protect from high-fat diet-induced metabolic disease.
“Additionally, higher NAD+ levels can promote the deacetylase and deacylase activity of both nuclear SIRT1 and mitochondrial SIRT3, which regulate mitochondrial function and protect from high-fat diet-induced metabolic disease42,81,85–88.”
From NAD+ metabolism and its roles in cellular processes during ageing (2021) · cites this paper as [81]
Multiple recent studies have shown that NAD+ supplements (NR and NMN), which can restore low NAD+ levels associated with ageing, are protective against obesity in rodent models.
“Additionally, multiple recent studies have shown that NAD+ supplements (NR and NMN), which can restore low NAD+ levels associated with ageing, are also protective against obesity in rodent models81,82,92, suggesting that these supplements could be explored as therapeutics to restore metabolic health in human patients with obesity.”
From NAD+ metabolism and its roles in cellular processes during ageing (2021) · cites this paper as [81]
Altering or disrupting metabolic status, for example by a high-fat diet, postpartum weight loss, or disruption of circadian rhythm, can lead to lower NAD+ levels and thereby reduced activity of sirtuins and other NAD+-dependent cellular processes.
“Altering or disrupting metabolic status, for example as a consequence of a high-fat diet81,82, postpartum weight loss83 and disruption of the circadian rhythm1,83, can lead to lower NAD+ levels, and thereby reduced activity of sirtuins as well as other NAD+-dependent cellular processes (see Supplementary Box 2 for details).”
From NAD+ metabolism and its roles in cellular processes during ageing (2021) · cites this paper as [81]
Exogenous NAD+ or precursor compounds that are converted to NAD+ in vivo can enhance tissue function and health.
“Addition of exogenous NAD+, or precursor compounds which are converted to NAD+ in vivo, is currently a hot topic in the field of aging biology due to recent successes in enhancing tissue function and health ((Yoshino et al. 2011), (Canto et al. 2012)).”
From The Mitochondrial Acylome Emerges: Proteomics, Regulation by Sirtuins, and Metabolic and Disease Implications (2018) · cites this paper as Canto et al. 2012
Increasing NAD+ by exogenous supplementation can protect against obesity in part by limiting mitochondrial acylation.
“As already described, increasing NAD+ by exogenous supplementation can protect against obesity ((Canto et al. 2012)) in part by limiting mitochondrial acylation - but can mitochondrial acylation actually cause the disease symptoms associated with excess calorie intake?”
From The Mitochondrial Acylome Emerges: Proteomics, Regulation by Sirtuins, and Metabolic and Disease Implications (2018) · cites this paper as Canto et al. 2012
NAD+ supplementation via its precursors nicotinamide riboside and nicotinamide mononucleotide enhances SIRT3 function in tissues such as skeletal muscle.
“Recently, NAD+ supplementation via its precursors nicotinamide riboside and nicotinamide mononucleotide has been shown to enhance SIRT3 function in tissues such as skeletal muscle ((Canto et al. 2012));”
From The Mitochondrial Acylome Emerges: Proteomics, Regulation by Sirtuins, and Metabolic and Disease Implications (2018) · cites this paper as Canto et al. 2012
The dosage scheme used in that study was insufficient to induce deacetylation in neurons.
“the dosage scheme used in this study was insufficient to induce deacetylation in neurons, but longer-term or higher-dose administration may yet offer the best path towards assisting SIRT3 in neuronal deacetylation.”
From The Mitochondrial Acylome Emerges: Proteomics, Regulation by Sirtuins, and Metabolic and Disease Implications (2018) · cites this paper as Canto et al. 2012
NR supplementation in mice increased mitochondrial to nuclear DNA ratios (a marker of mitochondrial mass).
“coupled to an increase in mitochondrial to nuclear DNA ratios (a marker of mitochondrial mass)”
From New strategies in sport nutrition to increase exercise performance (2016) · cites this paper as [171]
The metabolic action of NR supplementation was mediated through SIRT1.
“The authors proposed that the metabolic action of NR supplementation was mediated through SIRT1”
From New strategies in sport nutrition to increase exercise performance (2016) · cites this paper as [171]
Endurance capacity increased by ~25% in NR supplemented mice.
“endurance capacity also increased by ~25% in the NR supplemented mice”
From New strategies in sport nutrition to increase exercise performance (2016) · cites this paper as [171]
The adaptive response of C2C12 myotubes to NR supplementation was lost following SIRT1 siRNA mediated knockdown.
“the adaptive response of C2C12 myotubes to NR supplementation was lost following SIRT1 siRNA mediated knockdown.”
From New strategies in sport nutrition to increase exercise performance (2016) · cites this paper as [171]
The protection from high fat feeding by NR supplementation was principally through an increase in energy expenditure and a reduction in cholesterol levels.
“principally through an increase in energy expenditure and a reduction in cholesterol levels [171].”
From New strategies in sport nutrition to increase exercise performance (2016) · cites this paper as [171]
NR supplementation protected mice from the deleterious effects of 8 weeks high fat feeding.
“NR supplementation protected mice from the deleterious effects of 8 weeks high fat feeding”
From New strategies in sport nutrition to increase exercise performance (2016) · cites this paper as [171]
NR supplementation in mice increased mitochondrial protein content.
“and increased mitochondrial protein content.”
From New strategies in sport nutrition to increase exercise performance (2016) · cites this paper as [171]
NR supplementation appears capable of altering skeletal muscle NAD+ content which in turn increases skeletal muscle mitochondrial biogenesis through a SIRT1-dependent process.
“Thus NR supplementation appears capable of altering skeletal muscle NAD + content which in turn increases skeletal muscle mitochondrial biogenesis through a SIRT1-dependent process [171] (Figure 1).”
From New strategies in sport nutrition to increase exercise performance (2016) · cites this paper as [171]
NR feeding to mice (400 mg/kg/day) resulted in modest increases in skeletal muscle NAD+ (~5%) following 1-week supplementation.
“NR feeding to mice (400 mg/kg/day) resulted in modest increases in skeletal muscle NAD + (~5%) following 1-week supplementation [171].”
From New strategies in sport nutrition to increase exercise performance (2016) · cites this paper as [171]
NR supplementation in C2C12 myotubes increased NAD+ content.
“Recently, Canto et al (2012) who showed that NR supplementation in C2C12 myotubes increased NAD + content”
From New strategies in sport nutrition to increase exercise performance (2016) · cites this paper as [171]
Nicotinamide riboside, which is converted to nicotinamide mononucleotide via the NAD+ salvage pathway in eukaryote cells, can boost NAD+ synthesis and enhance oxidative metabolism and protect mouse tissues from high-fat diet-induced metabolic abnormalities by means of PPARγ and antioxidant gene upregulation.
“For instance, nicotinamide riboside, which is converted to nicotinamide mononucleotide via the NAD+ salvage pathway in eukaryote cells, can boost NAD+ synthesis and can enhance oxidative metabolism and protect mouse tissues from high-fat diet-induced metabolic abnormalities (264) by means of PPARγ and antioxidant gene upregulation (265).”
From Metabolic Flexibility as an Adaptation to Energy Resources and Requirements in Health and Disease (2018) · cites this paper as [264]
Nicotinamide mononucleotide and nicotinamide riboside increase mitochondrial function and improve glucose homeostasis in obese mice.
“Moreover, NMN252 and nicotinamide riboside255, another NAD+ precursor, increased mitochondrial function and improved glucose homeostasis in obese mice.”
From Mitochondrial and metabolic dysfunction in ageing and age-related diseases (2022) · cites this paper as [255]
Low NAD+ is a causal mechanism for mitochondrial perturbations in age-related pathologies in model organisms.
“However, low NAD+ is a causal mechanism for mitochondrial perturbations in age-related pathologies in model organisms49–51.”
From Mitochondrial oxidative capacity and NAD+ biosynthesis are reduced in human sarcopenia across ethnicities (2019) · cites this paper as [51]
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“The benefit of boosting NAD to induce Sirt1-dependent mitochondrial biogenesis, as presently observed with PARPi, was previously shown by our group by supplementing a HFHS diet with the NAD precursor NR [11,27,48].”
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“Nicotinamide has been shown to protect against oxidative stress and maintain mitochondrial health (Gomes et al., 2013; Mitchell et al., 2018), while its related compound, NR, was demonstrated to promote oxidative metabolism by means of increasing the NAD+/ NADH ratio (Canto et al., 2012).”
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NAD+ boosting reduces age-associated amyloidosis and restores mitochondrial homeostasis in muscle
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Aberrant protein acylation is a common observation in inborn errors of acyl-CoA metabolism
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- Authors
- Cantó, C., Houtkooper, R. H., Pirinen, E., Youn, D. Y., Oosterveer, M. H., Cen, Y., Fernandez-Marcos, P. J., Yamamoto, H., Andreux, P. A., Cettour-Rose, P., Gademann, K., Rinsch, C., Schoonjans, K., Sauve, A. A., & Auwerx, J.
- Affiliations
- École Polytechnique Fédérale de Lausanne (CH)
- University of Eastern Finland (FI)
- Weill Cornell Medicine (US)
- University of Basel (CH)
- Amazentis (Switzerland) (CH)
- Corresponding author
- Auwerx, Johan
- ORCID
- Venue
- Cell Metabolism
- Publisher
- Elsevier BV
- Published
- 2012-06
- Volume
- 15
- Issue
- 6
- Pages
- 838-847
- ISSN
- 1550-4131 (ISSN-L)
- PMC
- PMC3616313
- OpenAlex
- W2082393205
- Cited by
- 1,238
- References
- 42
- Citations by year
- 2026: 72 · 2025: 109 · 2024: 93 · 2023: 95 · 2022: 112 · 2021: 127 · 2020: 100 · 2019: 99 · 2018: 81 · 2017: 91 · 2016: 77 · 2015: 60 · 2014: 62 · 2013: 51 · 2012: 8
- FWCI
- 28.47
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Pure Amsterdam UMC (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- Infoscience (Ecole Polytechnique Fédérale de Lausanne) (submittedVersion)
- Infoscience (Ecole Polytechnique Fédérale de Lausanne) (submittedVersion, cc-by-nc-nd)
- University of Groningen research database (University of Groningen / Centre for Information Technology) (submittedVersion)
- Topics
- Health Sciences › Medicine › Geriatrics and Gerontology › Sirtuins and Resveratrol in Medicine
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Biochemical and Molecular Research
- Keywords
- nicotinamide riboside, NAD+ precursors, SIRT1, SIRT3, sirtuins, oxidative metabolism, high-fat diet-induced obesity, PARP1, CD38, mitochondrial function, metabolic disorders, dietary supplementation, aging
- MeSH terms
- Superoxide Dismutase 2, Acetylation, Animals, Brain, Adipose Tissue, Brown, Energy Metabolism, Humans, Liver, Male, Mice, Inbred C57BL, Mitochondria, NAD, Niacinamide, Obesity, Organ Specificity, Oxidation-Reduction, Oxygen Consumption, Protein Processing, Post-Translational, Pyridinium Compounds, Receptors, Nicotinic, Superoxide Dismutase, Weight Gain, Muscle, Skeletal, Dietary Supplements, Electron Transport Complex I, Receptors, G-Protein-Coupled, Mice, Sirtuin 1, Sirtuin 3, HEK293 Cells, Diet, High-Fat
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