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Study summary · NAD⁺, sirtuins & cellular energy

Can CD38 be pharmacologically inhibited to increase NAD+ levels and improve metabolic health?

In one paragraph

Apigenin Capsules, an animal study (Diabetes 2013, PMID 23172919) — treatment of cell cultures with apigenin decreased global acetylation, as well as the acetylation of p53 and RelA-p65. No numeric effect size is reported for Apigenin Capsules in the source abstract.

Source: Diabetes 2013, PMID 23172919 ↗ · Research map · How Magellan grades evidence · evidence confidence: low

Diabetes · 2013 · PMID 23172919 · DOI 10.2337/db12-1139

Plain-English summary written and published by Magellan Longevity · medical review by Gabriel Radu, DO (physiatrist, NPI 1376861765). We summarize what the paper reported — we did not run this study.

The takeaway

The flavonoid apigenin can inhibit the enzyme CD38, leading to increased NAD+ levels and improved metabolic health in obese mice.

The question

Can CD38 be pharmacologically inhibited to increase NAD+ levels and improve metabolic health?

What they tested

Inhibiting CD38 will increase cellular NAD+ levels, activate sirtuins, decrease protein acetylation, and improve metabolic syndrome parameters.

How they did it

The study investigated the role of CD38 in regulating protein acetylation via NAD+ levels and sirtuin activity. It characterized quercetin and apigenin as CD38 inhibitors. Cell cultures were treated with apigenin to observe changes in NAD+ levels and protein acetylation. Obese mice were administered apigenin to assess its effects on NAD+ levels, protein acetylation, and glucose and lipid homeostasis.

What they found

CD38 regulates global protein acetylation through changes in NAD+ levels and sirtuin activity. Pharmacological inhibition of CD38 by apigenin resulted in higher intracellular NAD+ levels in cell cultures. Treatment of cell cultures with apigenin decreased global acetylation, as well as the acetylation of p53 and RelA-p65. Apigenin administration to obese mice increased NAD+ levels, decreased global protein acetylation, and improved several aspects of glucose and lipid homeostasis.

What it means

CD38 is a novel pharmacological target for treating metabolic diseases through NAD+-dependent pathways, with apigenin demonstrating efficacy as a CD38 inhibitor.

Limitations

The abstract does not explicitly state any limitations of the study.

Where the published abstract does not list limitations, we say so rather than inventing them. Read the full paper on PubMed before drawing conclusions.

“apigenin increases NAD+ levels by inhibiting CD38”— from the published abstract, Diabetes 2013

The paper at a glance

TitleFlavonoid apigenin is an inhibitor of the NAD+ ase CD38: implications for cellular NAD+ metabolism
JournalDiabetes
Year2013
PMID23172919 ↗
DOI10.2337/db12-1139 ↗
TopicNAD⁺, sirtuins & cellular energy

Read the source: PubMed record (authors, abstract, full citation) ↗ · Publisher via doi.org ↗

Where Magellan uses this paper

This citation sits behind the evidence grade on the pages below. Grades are set from the research and are independent of affiliate commissions.

Apigenin Capsules

CD38 activity rises with age and drives the tissue decline of NAD+ that is linked to mitochondrial dysfunction, inflammation, and cellular senescence, so inhibiting CD38 is a plausible strategy to preserve NAD+ during aging.

Apigenin Capsules

Apigenin (4',5,7-trihydroxyflavone) is a naturally occurring flavone abundant in chamomile, parsley…

Check price on Amazon ↗

Research describes the compound or intervention studied. It is not a claim about any specific product.

Molecules & mechanisms in this paper

Each of these is named in the paper’s own words above. Open the monograph for the full mechanism and its other citations.

QuercetinApigeninCD38NAD⁺

Cite this page

These citations point at this summary. To cite the original paper with its full author list, use the PubMed record or doi.org.

APA
Magellan Longevity. (2026). Can CD38 be pharmacologically inhibited to increase NAD+ levels and improve metabolic health? [Plain-English summary of Diabetes 2013, PMID 23172919, DOI 10.2337/db12-1139]. Magellan Longevity. https://magellanlongevity.com/study/d23172919.html
BibTeX
@misc{magellan_d23172919, title = {Can CD38 be pharmacologically inhibited to increase NAD+ levels and improve metabolic health?}, author = {{Magellan Longevity}}, year = {2026}, howpublished = {\url{https://magellanlongevity.com/study/d23172919.html}}, note = {Plain-English summary of PubMed PMID 23172919; DOI 10.2337/db12-1139; Diabetes 2013. Reviewed by Gabriel Radu, DO}, urldate = {2026-08-11} }
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How this summary was made. Every section above restates what the published abstract of PMID 23172919 reports — the question, the design, the numbers, the authors’ own conclusion and their stated limitations. We do not add claims the paper did not make, and we keep negative and no-effect findings in. Magellan’s evidence grades are set from research like this and never from affiliate commissions.

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Educational information, not medical advice. This is a plain-English summary of published research; it is not a treatment recommendation and nothing here is intended to diagnose, treat, cure, or prevent any disease. Individual studies can be wrong, and a single paper rarely settles a question. Talk to your physician before acting on any research, especially if you are pregnant, nursing, or taking medication.