Nicotinamide mononucleotide protects against pro-inflammatory cytokine-mediated impairment of mouse islet function
Open accessAbstract
Aims/hypothesis Nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme for NAD(+) biosynthesis, exists as intracellular NAMPT (iNAMPT) and extracellular NAMPT (eNAMPT). eNAMPT, secreted from adipose tissue, promotes insulin secretion. Administration of nicotinamide mononucleotide (NMN), a product of the eNAMPT reaction, corrects impaired islet function in Nampt ( +/- ) mice. One of its potential targets is the NAD(+)-dependent deacetylase sirtuin 1. We hypothesised that altered NAMPT activity might contribute to the suppression of islet function associated with inflammation, and aimed to determine whether NMN could improve cytokine-mediated islet dysfunction.Methods Acute effects of NMN on cytokine-mediated islet dysfunction were examined in islets incubated with TNFα and IL1β, and in mice fed a fructose-rich diet (FRD) for 16 weeks. Changes in iNAMPT, eNAMPT and inflammation levels were determined in FRD-fed mice.Results FRD-fed mice displayed markedly lower levels of circulating eNAMPT, with impaired insulin secretion and raised islet expression of Il1b. NMN administration lowered Il1b expression and restored suppressed insulin secretion in FRD-fed mice. NMN also restored insulin secretion in islets cultured with pro-inflammatory cytokines. The changes in islet function corresponded with changes in key markers of islet function and differentiation. The anti-inflammatory effects of NMN were partially blocked by inhibition of sirtuin 1.Conclusions/interpretation Chronic fructose feeding causes severe islet dysfunction in mice. Onset of beta cell failure in FRD-fed mice may occur via lowered secretion of eNAMPT, leading to increased islet inflammation and impaired beta cell function. Administration of exogenous NMN to FRD-fed mice corrects inflammation-induced islet dysfunction. Modulation of this pathway may be an attractive target for amelioration of islet dysfunction associated with inflammation.
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NMN 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 [20]
The Results and Discussion (page unavailable) report that NMN reduced an inflammatory marker and restored impaired insulin secretion in fructose-fed mice and cytokine-exposed islets. This supports a limited claim about NMN, islet inflammation, and diabetes-related dysfunction—not protection against diabetes itself. The paper does not establish protective effects of NR or address Alzheimer disease or endothelial dysfunction. (LLM, conf=0.89)
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 [20]
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 measuredNMN (100 μmol/l) restored insulin secretion in islets cultured with IL1β and TNFα in a partially SIRT1-dependent manner.
“In this case, NMN administration (100 μmol/l) restored insulin secretion in islets cultured with pro-inflammatory cytokines IL1β and TNFα, in a partially SIRT1-dependent manner.”
From NAD+ Precursors Nicotinamide Mononucleotide (NMN) and Nicotinamide Riboside (NR): Potential Dietary Contribution to Health (2023) · cites this paper as [20]
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- Authors
- Caton, P. W., Kieswich, J., Yaqoob, M. M., Holness, M. J., & Sugden, M. C.
- Affiliations
- Queen Mary University of London (GB)
- Corresponding author
- Caton, P. W.
- Venue
- Diabetologia
- Published
- 2011-09-08
- Volume
- 54
- Issue
- 12
- Pages
- 3083-3092
- ISSN
- 0012-186X (ISSN-L)
- 1432-0428
- OpenAlex
- W1995579184
- Cited by
- 140
- References
- 41
- Citations by year
- 2026: 8 · 2025: 11 · 2024: 8 · 2023: 19 · 2022: 14 · 2021: 10 · 2020: 10 · 2019: 11 · 2018: 7 · 2017: 8 · 2016: 9 · 2015: 4 · 2014: 6 · 2013: 11 · 2012: 4
- FWCI
- 6.87
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Diabetologia (publishedVersion)
- PubMed (publishedVersion)
- Research Portal (King's College London) (submittedVersion)
- Funders
- Queen Mary University of London
- Diabetes UK
- Topics
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Health Sciences › Medicine › Geriatrics and Gerontology › Sirtuins and Resveratrol in Medicine
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Keywords
- nicotinamide mononucleotide, visfatin, extracellular NAMPT, SIRT1, islet dysfunction, beta-cell failure, insulitis, inflammatory cytokines, TNF-α, IL-1β, high-fructose diet, insulin secretion, NAD biosynthesis, type 2 diabetes
- MeSH terms
- Insulin Secretion, Animals, Cell Differentiation, Cells, Cultured, Fructose, Inflammation, Insulin, Islets of Langerhans, Male, Mice, Inbred C57BL, Nicotinamide Mononucleotide, Tumor Necrosis Factor-alpha, Cytokines, Mice, Interleukin-1beta, Nicotinamide Phosphoribosyltransferase, Sirtuin 1
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