Nicotinamide Mononucleotide, a Key NAD+ Intermediate, Treats the Pathophysiology of Diet- and Age-Induced Diabetes in Mice
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Type 2 diabetes (T2D) has become epidemic in our modern lifestyle, likely due to calorie-rich diets overwhelming our adaptive metabolic pathways. One such pathway is mediated by nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in mammalian NAD(+) biosynthesis, and the NAD(+)-dependent protein deacetylase SIRT1. Here, we show that NAMPT-mediated NAD(+) biosynthesis is severely compromised in metabolic organs by high-fat diet (HFD). Strikingly, nicotinamide mononucleotide (NMN), a product of the NAMPT reaction and a key NAD(+) intermediate, ameliorates glucose intolerance by restoring NAD(+) levels in HFD-induced T2D mice. NMN also enhances hepatic insulin sensitivity and restores gene expression related to oxidative stress, inflammatory response, and circadian rhythm, partly through SIRT1 activation. Furthermore, NAD(+) and NAMPT levels show significant decreases in multiple organs during aging, and NMN improves glucose intolerance and lipid profiles in age-induced T2D mice. These findings provide critical insights into a potential nutriceutical intervention against diet- and age-induced T2D.
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Under stress conditions, NAD+ biosynthesis and NAD+ levels decrease while the activity of NAD-consuming enzymes increases.
“In stress conditions, NAD+ biosynthesis and levels decrease as well as the activity of consuming enzymes rises.”
From NAD+ Precursors Nicotinamide Mononucleotide (NMN) and Nicotinamide Riboside (NR): Potential Dietary Contribution to Health (2023) · cites this paper as [13]
The Results report that inflammatory and oxidative-stress treatments reduced NAMPT and NAD+ levels in primary hepatocytes, and the Discussion links reduced NAD+ biosynthesis to inflammation or oxidative stress. The paper does not report a rise in NAD-consuming enzyme activity under those conditions; its Results instead suggest that SIRT1 activity is suppressed by a high-fat diet. No page numbers are available in our copy. (LLM, conf=0.88)
Experimental — accuracy not yet measuredNMN and NR protect against diabetes, Alzheimer disease, endothelial dysfunction, and inflammation.
“NMN and NR demonstrated protect against diabetes, Alzheimer disease, endothelial dysfunction, and inflammation.”
From NAD+ Precursors Nicotinamide Mononucleotide (NMN) and Nicotinamide Riboside (NR): Potential Dietary Contribution to Health (2023) · cites this paper as [13]
The Results and Discussion (page unavailable) report that NMN improved glucose tolerance in diet- and age-induced diabetic mice and reversed inflammatory-response gene-expression changes. They do not show that NR protects against these conditions; NR was measured after NMN administration, not tested as a treatment. The paper also does not establish protection against Alzheimer disease or endothelial dysfunction, or demonstrate prevention of inflammation as a clinical condition. (LLM, conf=0.90)
Experimental — accuracy not yet measuredNAD+ synthesis can occur from tryptophan and vitamin B3, and NR and NMN also promote NAD+ synthesis.
“NAD+ synthesis can occur from tryptophan and vitamin B3 (niacin and nicotinamide). Later, the intermediates NR and NMN have also been identified to promote NAD+ synthesis [13, 55].”
From NAD+ Precursors Nicotinamide Mononucleotide (NMN) and Nicotinamide Riboside (NR): Potential Dietary Contribution to Health (2023) · cites this paper as [13]
The Results section (page not supplied) shows that administered NMN was converted to NAD+ and enhanced NAD+ biosynthesis. It reports an increase in NR after NMN administration, but does not establish that NR itself promotes NAD+ synthesis. The citation is attached to the sentence about NR and NMN, not the preceding sentence about tryptophan and vitamin B3. (LLM, conf=0.88)
Experimental — accuracy not yet measuredNAMPT protein and NAD+ levels decrease significantly in white adipose tissue and skeletal muscle of old mice, affecting NAD-dependent enzymes such as sirtuins.
“The NAMPT (nicotinamide phosphoribosyltransferase) protein and NAD+ levels decreased significantly in organs, such as white adipose tissue and skeletal muscle in old mice [13] affecting the activity of NAD+ -dependent enzymes such as sirtuins [15, 98].”
From NAD+ Precursors Nicotinamide Mononucleotide (NMN) and Nicotinamide Riboside (NR): Potential Dietary Contribution to Health (2023) · cites this paper as [13]
The Results section on age-induced diabetes reports significant NAD+ decreases in white adipose tissue and skeletal muscle of old mice and says NAMPT protein levels also decreased in those tissues. It does not state that the NAMPT decreases were statistically significant. The sirtuin-activity clause is attached to different citations, so it is not assessed here; no page number is available in our copy. (LLM, conf=0.85)
Experimental — accuracy not yet measuredNMN has been proposed as a nutraceutical to prevent age-related physiological decline and has been shown to improve diabetes and Alzheimer disease, enhance aerobic capacity, and exert cardio- and vasoprotective, anti-inflammatory, antioxidant, endothelial-protective, heart failure-protective, and ischemia/reperfusion-protective effects.
“Proposed as a nutraceutical to prevent age-related physiological decline [1••, 91], NMN has shown to improve diabetes [13, 20, 38] and Alzheimer’s disease [22, 23], enhance aerobic capacity [92], and exhibit cardio- and vasoprotective actions. It inhibits inflammation and decreases oxidative stress, preventing arterial and endothelial dysfunction [32, 93], and protecting against heart failure [94]”
From NAD+ Precursors Nicotinamide Mononucleotide (NMN) and Nicotinamide Riboside (NR): Potential Dietary Contribution to Health (2023) · cites this paper as [13]
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measured
Under disturbed nutrient conditions such as high-fat and high-protein intake, NAD+ levels decrease.
“Under disturbed nutrient conditions, such as high-fat and -protein intake, NAD+ levels decreases [12, 13].”
From NAD+ Precursors Nicotinamide Mononucleotide (NMN) and Nicotinamide Riboside (NR): Potential Dietary Contribution to Health (2023) · cites this paper as [13]
The Results section, “NAMPT-mediated NAD+ biosynthesis is compromised by HFD” (page unavailable), reports reduced NAD+ in the liver and white adipose tissue of high-fat-diet-fed diabetic mice, but not in skeletal muscle. The paper does not establish a decrease with high-protein intake, and the claim omits the study’s mouse and tissue-specific limits. (LLM, conf=0.88)
Experimental — accuracy not yet measuredIn diet- and age-induced diabetic models, intraperitoneal NMN (500 mg/kg/day for 11 days) ameliorated impaired glucose tolerance substantially and enhanced hepatic insulin sensitivity.
“In both diet- and age-induced diabetic models, the administration of NMN via intraperitoneal (500 mg/kg body weight/day for 11 days) ameliorated impaired glucose tolerance substantially and enhanced hepatic insulin sensitivity.”
From NAD+ Precursors Nicotinamide Mononucleotide (NMN) and Nicotinamide Riboside (NR): Potential Dietary Contribution to Health (2023) · cites this paper as [13]
The Results report improved glucose tolerance in diet- and age-induced diabetic mice and improved hepatic insulin sensitivity in HFD-fed diabetic females. The 500 mg/kg/day intraperitoneal dose is supported, but 11 injections were used for aged diabetic females; HFD-fed males and females received 10 and 7 days, respectively, and aged diabetic males improved after one dose. The claim also extends the hepatic insulin-sensitivity finding beyond the females in whom it was assessed. Page numbers are not available in the supplied passages. (LLM, conf=0.90)
Experimental — accuracy not yet measuredUsing one-dimensional HPLC-based methods, NMN intracellular concentrations were reported to rise up to ~400-500 pmol mg−1 of white adipose and pancreatic tissue 15 min after intraperitoneal injection of 500 mg kg−1 of NMN, parallel to a peak level of NAD+ in white adipose tissue of ~50 pmol mg−1.
“For example, using one-dimensional HPLC-based methods, NMN intracellular concentrations were reported to rise up to ∼400–500 pmol mg−1 of white adipose and pancreatic tissue 15 min after intraperitoneal injection of 500 mg kg−1 of NMN, parallel to a peak level of NAD+ in white adipose tissue of ∼50 pmol mg−1 (ref. 9).”
From NRK1 controls nicotinamide mononucleotide and nicotinamide riboside metabolism in mammalian cells (2016) · cites this paper as [9]
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredNAD+ levels decrease in various tissues during aging and play a critical role in the pathophysiology of age-associated metabolic disorders, neurodegenerative diseases, and mental disorders.
“It is recognized the decrease of NAD+ levels in various tissues during aging [11, 13, 96, 97], playing a critical role in the pathophysiology of several diseases, including age-associated metabolic disorders, neurodegenerative diseases, and mental disorders [14].”
From NAD+ Precursors Nicotinamide Mononucleotide (NMN) and Nicotinamide Riboside (NR): Potential Dietary Contribution to Health (2023) · cites this paper as [13]
A significant cause of age-associated NAD+ decline is decreased NAMPT-mediated biosynthesis.
“A significant cause for this age-associated NAD+ decline is the decrease in NAMPT-mediated biosynthesis.”
From NAD+ Precursors Nicotinamide Mononucleotide (NMN) and Nicotinamide Riboside (NR): Potential Dietary Contribution to Health (2023) · cites this paper as [13]
Reversing changes in gene expression related to oxidative stress, inflammatory response, and circadian rhythm was in part a result of SIRT1 activation.
“The indicated reversing changes in gene expression related to oxidative stress, inflammatory response, and circadian rhythm was in part a result of SIRT1 activation [13].”
From NAD+ Precursors Nicotinamide Mononucleotide (NMN) and Nicotinamide Riboside (NR): Potential Dietary Contribution to Health (2023) · cites this paper as [13]
Mice receiving a high-fat diet have increased inflammation, which drives decreased expression of NAMPT and reduced activity of the NAD+ salvage pathway, providing a potential mechanistic explanation for why NAD+ levels decline during obesity.
“Additionally, mice receiving a high-fat diet have increased inflammation, which drives decreased expression of NAMPT, and reduced activity of the NAD+ salvage pathway82 (BOX 1), providing a potential mechanistic explanation for why NAD+ levels decline during obesity.”
From NAD+ metabolism and its roles in cellular processes during ageing (2021) · cites this paper as [82]
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 [82]
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 [82]
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 Yoshino et al. 2011
Nicotinamide mononucleotide supplementation restores β-cell glucose-stimulated insulin secretion and hepatic and skeletal muscle insulin sensitivity in mouse models with impaired glucose homeostasis.
“Supplementation of the precursor nicotinamide mononucleotide (NMN) re-established β-cell glucose-stimulated insulin secretion as well as hepatic and skeletal muscle insulin sensitivity in mouse models with impaired glucose homeostasis252,253.”
From Mitochondrial and metabolic dysfunction in ageing and age-related diseases (2022) · cites this paper as [252]
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 [252]
HFD reduces NAD+ content in diverse tissues.
“HFD also reduces the NAD+ content in diverse tissues, which is likely to impair SIRT1 activation (Kim et al, 2011; Yoshino et al, 2011) (Fig 3B).”
From Mitochondrial response to nutrient availability and its role in metabolic disease (2014) · cites this paper as Yoshino et al, 2011
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BackgroundInfluentialTelomere Dysfunction Induces Sirtuin Repression that Drives Telomere-Dependent Disease
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- Authors
- Yoshino, J., Mills, K. F., Yoon, M. J., & Imai, S.-I.
- Affiliations
- Washington University in St. Louis (US)
- Corresponding author
- Imai, Shin-ichiro
- Venue
- Cell Metabolism
- Publisher
- Elsevier BV
- Published
- 2011-10
- Volume
- 14
- Issue
- 4
- Pages
- 528-536
- ISSN
- 1550-4131 (ISSN-L)
- PMC
- PMC3204926
- OpenAlex
- W2038011036
- Cited by
- 1,340
- References
- 27
- Citations by year
- 2026: 65 · 2025: 98 · 2024: 129 · 2023: 127 · 2022: 145 · 2021: 133 · 2020: 98 · 2019: 111 · 2018: 88 · 2017: 82 · 2016: 76 · 2015: 55 · 2014: 61 · 2013: 51 · 2012: 19
- FWCI
- 20.43
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 655 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Cell Metabolism (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Aging (AG02150)
- Ellison Medical Foundation
- Longer Life Foundation
- Japan Research Foundation for Clinical Pharmacology
- Manpei Suzuki Diabetes Foundation
- Kanae Foundation for the Promotion of Medical Science
- Topics
- Health Sciences › Medicine › Geriatrics and Gerontology › Sirtuins and Resveratrol in Medicine
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Keywords
- nicotinamide mononucleotide, NAD biosynthesis, visfatin, SIRT1, type 2 diabetes, high-fat diet, aging, impaired glucose tolerance, hepatic insulin sensitivity, oxidative stress, inflammation, circadian rhythm
- MeSH terms
- Aging, Animals, Circadian Rhythm, Diabetes Mellitus, Type 2, Disease Models, Animal, Gene Expression Regulation, Glucose, Hypoglycemic Agents, Insulin, NAD, Nicotinamide Mononucleotide, Cytokines, Oxidative Stress, Lipid Metabolism, Mice, Nicotinamide Phosphoribosyltransferase, Sirtuin 1, Diet, High-Fat
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