The Claim
Pharmacological inhibition of CD38 by apigenin in obese mice increases hepatic NAD+ levels and reduces global protein acetylation, which is associated with enhanced expression of fatty acid oxidation enzymes and decreased liver triglyceride content.
What the research says
Supports is higher
Support is ahead, but a single strong opposing study can change this.
These are independent scores, not a percentage. Higher-grade studies count more, so a single strong opposing study can outweigh several weaker ones.
In obese mice, a compound called apigenin inhibits the CD38 enzyme, leading to higher levels of NAD+ in the liver, lower levels of protein acetylation, increased activity of enzymes that break down fatty acids, and reduced fat accumulation in the liver.
See the scientific wording
Pharmacological inhibition of CD38 by apigenin in obese mice increases hepatic NAD+ levels and reduces global protein acetylation, which is associated with enhanced expression of fatty acid oxidation enzymes and decreased liver triglyceride content.
A compound blocks an enzyme that breaks down NAD+, causing NAD+ levels to rise in the liver. Higher NAD+ turns on a protein that removes acetyl groups from other proteins involved in fat burning. This turns on genes that break down fatty acids, so the liver burns more fat and stores less triglyceride.
What the research says
1 studyStudy: Flavonoid Apigenin Is an Inhibitor of the NAD+ase CD38
In obese mice, giving a natural compound called apigenin blocks an enzyme (CD38) that breaks down NAD+, a molecule important for metabolism. This causes more NAD+ to build up in the liver, which helps clean up excess fat by turning on fat-burning genes — resulting in significantly less fat in the liver.
Score breakdown, mechanism chain, raw evidence, ideal studies needed & 1 supporting studies
Not medical advice. For informational purposes only. Always consult a qualified healthcare professional before making health decisions.