Flavonoid apigenin is an inhibitor of the NAD+ ase CD38: implications for cellular NAD+ metabolism, protein acetylation, and treatment of metabolic syndrome.
Level 5 - mechanism / opinion, no new human data
Preclinical in vitro cell culture and animal (mouse) study with no human clinical data.
PubMed 23172919 · doi:10.2337/db12-1139
What was done
The authors characterized the flavonoids quercetin and apigenin as pharmacological inhibitors of the NAD+ase enzyme CD38. They evaluated the effects of CD38 inhibition and apigenin treatment on cellular NAD+ levels, sirtuin activity, and global and target-specific protein acetylation (including p53 and RelA-p65) in cell culture models. They subsequently administered apigenin to obese mice to assess its impact on tissue NAD+ levels, protein acetylation patterns, and parameters of glucose and lipid homeostasis.
What was found
Pharmacological inhibition of CD38 with apigenin elevated intracellular NAD+ levels and reduced global protein acetylation as well as p53 and RelA-p65 acetylation in cell cultures. In obese mice, apigenin administration increased NAD+ levels, decreased global protein acetylation, and improved measures of glucose and lipid homeostasis. The abstract reports qualitative directions of effect without providing specific numerical values, sample sizes, or effect sizes.
Why it matters
This study identifies CD38 as an actionable pharmacological target for boosting cellular NAD+ levels and demonstrates that dietary flavonoids like apigenin can inhibit CD38 to improve metabolic endpoints in preclinical models.
Limits
The study was conducted exclusively in cell cultures and obese mouse models, so the findings cannot be directly extrapolated to humans. Specific sample sizes, dosages, pharmacokinetic parameters, and quantitative outcome measurements (such as blood glucose, insulin, lipid concentrations, or exact fold changes) are not provided in the abstract.
Cited by
- supports Apigenin, fisetin, and quercetin inhibit the enzyme CD38 (NADase).