Cited by 332Sirtuins and Resveratrol in MedicineNatural Antidiabetic Agents StudiesBiochemical and Molecular Research

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Flavonoid Apigenin Is an Inhibitor of the NAD+ase CD38

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Escande, Carlos, Nin, Veronica, Price, Nathan L., Capellini, Verena, Gomes, Ana P., Barbosa, Maria Thereza, O’Neil, Luke, White, Thomas A., Sinclair, David A., Chini, Eduardo N.·2013·Diabetes

DOI 10.2337/db12-1139PMC PMC3609577

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Abstract

Metabolic syndrome is a growing health problem worldwide. It is therefore imperative to develop new strategies to treat this pathology. In the past years, the manipulation of NAD+ metabolism has emerged as a plausible strategy to ameliorate metabolic syndrome. In particular, an increase in cellular NAD+ levels has beneficial effects, likely because of the activation of sirtuins. Previously, we reported that CD38 is the primary NAD+ase in mammals. Moreover, CD38 knockout mice have higher NAD+ levels and are protected against obesity and metabolic syndrome. Here, we show that CD38 regulates global protein acetylation through changes in NAD+ levels and sirtuin activity. In addition, we characterize two CD38 inhibitors: quercetin and apigenin. We show that pharmacological inhibition of CD38 results in higher intracellular NAD+ levels and that treatment of cell cultures with apigenin decreases global acetylation as well as the acetylation of p53 and RelA-p65. Finally, apigenin administration to obese mice increases NAD+ levels, decreases global protein acetylation, and improves several aspects of glucose and lipid homeostasis. Our results show that CD38 is a novel pharmacological target to treat metabolic diseases via NAD+-dependent pathways.

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Authors: Escande, C., Nin, V., Price, N. L., Capellini, V., Gomes, A. P., Barbosa, M. T., O’Neil, L., White, T. A., Sinclair, D. A., & Chini, E. N.
Affiliations: Mayo Clinic (US)
Department of Anesthesiology and Kogod Aging Center Mayo Clinic, Rochester, Minnesota
Harvard University (US)
Corresponding author: Chini, Eduardo N.
ORCID: Escande, Carlos
Price, Nathan L.
Capellini, Verena
Barbosa, Maria Thereza
White, Thomas A.
Sinclair, David A.
Chini, Eduardo N.
Venue: Diabetes
Publisher: American Diabetes Association
Published: 2013-03-14
Volume: 62
Issue: 4
Pages: 1084-1093
ISSN: 0012-1797 (ISSN-L)
1939-327X
DOI: 10.2337/db12-1139
PMC: PMC3609577
OpenAlex: W2112866277
Cited by: 332
References: 48
Citations by year: 2026: 27 · 2025: 20 · 2024: 30 · 2023: 17 · 2022: 37 · 2021: 38 · 2020: 33 · 2019: 23 · 2018: 31 · 2017: 25 · 2016: 17 · 2015: 18 · 2014: 11 · 2013: 5
FWCI: 5.35
Type: journal article
Language: en
Update notices: correction (2014-04-01)
Open access: hybrid
doi.org
Licence: cc-by-nc-nd
creativecommons.org/licenses/by-nc-nd/3.0/ (vor, 3089 d)
Locations: Diabetes (publishedVersion, cc-by-nc-nd)
Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-nd)
PubMed Central (publishedVersion, cc-by-nc-nd)
PubMed (publishedVersion)
Digital Access to Scholarship at Harvard (DASH) (Harvard University) (submittedVersion, cc-by)
Funders: National Institute on Aging (R37AG028730, T32AG000222)
National Institute of Diabetes and Digestive and Kidney Diseases (P30DK050456, R01DK084055)
Topics: Health Sciences › Medicine › Geriatrics and Gerontology › Sirtuins and Resveratrol in Medicine
Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Natural Antidiabetic Agents Studies
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Biochemical and Molecular Research
Keywords: apigenin, CD38, NAD+ metabolism, sirtuins, protein acetylation, quercetin, metabolic syndrome, obesity, p53 acetylation, glucose homeostasis, lipid homeostasis, flavonoids, CD38 inhibitors
MeSH terms: Animals, Gene Expression Regulation, Humans, Mice, Inbred C57BL, NAD, Obesity, Quercetin, Random Allocation, Molecular Structure, Mice, Knockout, Metabolic Syndrome, Cell Line, Tumor, Apigenin, Mice, ADP-ribosyl Cyclase 1, Sirtuin 1

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Flavonoid Apigenin Is an Inhibitor of the NAD+ase CD38

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