Cited by 140Pancreatic function and diabetesSirtuins and Resveratrol in MedicineDiabetes Treatment and Management

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Nicotinamide mononucleotide protects against pro-inflammatory cytokine-mediated impairment of mouse islet function

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Caton, P. W., Kieswich, J., Yaqoob, M. M., Holness, M. J., Sugden, M. C.·2011·Diabetologia

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Abstract

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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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.
ORCID: Caton, P. W.
Kieswich, J.
Venue: Diabetologia
Publisher: Springer Science and Business Media LLC
Published: 2011-09-08
Volume: 54
Issue: 12
Pages: 3083-3092
ISSN: 0012-186X (ISSN-L)
1432-0428
DOI: 10.1007/s00125-011-2288-0
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 › Endocrinology, Diabetes and Metabolism › 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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Nicotinamide mononucleotide protects against pro-inflammatory cytokine-mediated impairment of mouse islet function

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