Evidence for a Direct Effect of the NAD+ Precursor Acipimox on Muscle Mitochondrial Function in Humans
Open accessAbstract
Recent preclinical studies showed the potential of nicotinamide adenine dinucleotide (NAD+) precursors to increase oxidative phosphorylation and improve metabolic health, but human data are lacking. We hypothesize that the nicotinic acid derivative acipimox, an NAD+ precursor, would directly affect mitochondrial function independent of reductions in nonesterified fatty acid (NEFA) concentrations. In a multicenter randomized crossover trial, 21 patients with type 2 diabetes (age 57.7 ± 1.1 years, BMI 33.4 ± 0.8 kg/m2) received either placebo or acipimox 250 mg three times daily dosage for 2 weeks. Acipimox treatment increased plasma NEFA levels (759 ± 44 vs. 1,135 ± 97 μmol/L for placebo vs. acipimox, P < 0.01) owing to a previously described rebound effect. As a result, skeletal muscle lipid content increased and insulin sensitivity decreased. Despite the elevated plasma NEFA levels, ex vivo mitochondrial respiration in skeletal muscle increased. Subsequently, we showed that acipimox treatment resulted in a robust elevation in expression of nuclear-encoded mitochondrial gene sets and a mitonuclear protein imbalance, which may indicate activation of the mitochondrial unfolded protein response. Further studies in C2C12 myotubes confirmed a direct effect of acipimox on NAD+ levels, mitonuclear protein imbalance, and mitochondrial oxidative capacity. To the best of our knowledge, this study is the first to demonstrate that NAD+ boosters can also directly affect skeletal muscle mitochondrial function in humans.
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The study was approved by the institutional medical ethics committee and registered at ClinicalTrials.gov and the Dutch trial register.
“The participants included in this study were derived from previous studies all performed at Maastricht University, approved by the institutional medical ethics committee and registered at ClinicalTrials.gov (NCT00943059 and NCT01298375) and in the Dutch trial register (https://www.trialregister.nl/trial/1888) [23–26].”
From Human skeletal muscle mitochondrial dynamics in relation to oxidative capacity and insulin sensitivity (2021) · cites this paper as [25]
The Research Design and Methods > Subjects section states that the Maastricht University Medical Ethics Committee approved this study. It does not report registration at ClinicalTrials.gov or the Dutch trial register, and Research Design and Methods describes participants recruited in both Maastricht and Düsseldorf, not solely at Maastricht University. No page number is available in our copy. (LLM, conf=0.88)
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- Authors
- van de Weijer, T., Phielix, E., Bilet, L., Williams, E. G., Ropelle, E. R., Bierwagen, A., Livingstone, R., Nowotny, P., Sparks, L. M., Paglialunga, S., Szendroedi, J., Havekes, B., Moullan, N., Pirinen, E., Hwang, J.-H., Schrauwen-Hinderling, V. B., Hesselink, M. K. C., Auwerx, J., Roden, M., & Schrauwen, P.
- Affiliations
- Department of Human Biology, Maastricht University Medical Center, Maastricht, the Netherlands
- Maastricht University Medical Centre (NL)
- École Polytechnique Fédérale de Lausanne (CH)
- Deutsches Diabetes-Zentrum e.V. (DE)
- Düsseldorf University Hospital (DE)
- University of Eastern Finland (FI)
- Institute for Clinical Diabetology, German Diabetes Center, Düsseldorf, Germany
- School for Nutrition, Toxicology and Metabolism, Maastricht University Medical Center, Maastricht, the Netherlands
- Corresponding author
- Roden, Michael
- Schrauwen, Patrick
- ORCID
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2014-10-28
- Volume
- 64
- Issue
- 4
- Pages
- 1193-1201
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- PMC
- PMC4375076
- OpenAlex
- W2038391272
- Cited by
- 139
- References
- 43
- Citations by year
- 2026: 2 · 2025: 15 · 2024: 10 · 2023: 15 · 2022: 16 · 2021: 13 · 2020: 15 · 2019: 11 · 2018: 8 · 2017: 14 · 2016: 10 · 2015: 9
- FWCI
- 5.61
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Diabetes (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Open Repository and Bibliography (University of Luxembourg) (submittedVersion, cc-by-nc-sa)
- Research Publications (Maastricht University) (submittedVersion, other-oa)
- Infoscience (Ecole Polytechnique Fédérale de Lausanne) (submittedVersion)
- Infoscience (Ecole Polytechnique Fédérale de Lausanne) (submittedVersion, cc-by-nc-nd)
- Funders
- École Polytechnique Fédérale de Lausanne
- Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (140780)
- Nierstichting (01C-104)
- Diabetes Fonds (01C-104)
- Nederlandse Organisatie voor Wetenschappelijk Onderzoek (918.96.618)
- Center for Translational Molecular Medicine (01 C-104)
- National Institutes of Health
- Health Science Center, University of Tennessee
- National Institute on Aging (R01AG043930)
- 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 › Mitochondrial Function and Pathology
- Keywords
- acipimox, NAD+ precursors, nicotinic acid, skeletal muscle mitochondrial function, type 2 diabetes, free fatty acids, mitochondrial respiration, mitochondrial unfolded protein response, nuclear-encoded mitochondrial genes, insulin sensitivity, C2C12 myotubes, mitochondrial oxidative capacity
- MeSH terms
- Hypolipidemic Agents, Diabetes Mellitus, Type 2, Female, Humans, Insulin Resistance, Male, Middle Aged, Mitochondria, Muscle, Pyrazines, Muscle, Skeletal, Cross-Over Studies
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