Study analysis · Diabetes · 2013
This plant compound could be the secret to burning fat and reversing fatty liver—without dieting.
A natural chemical in parsley and celery blocks an enzyme that drains energy from your cells, helping obese mice burn fat and control blood sugar.
Overview
What the study found
The study in plain English — the bottom line, every takeaway we extracted, and what to do with them.
In simple terms
This study showed that a chemical in plants called apigenin can block a specific enzyme in mice and lab cells, which then made their bodies produce more of a helpful molecule called NAD+. That helped their blood sugar and fat levels improve. But this doesn’t mean eating apigenin will fix obesity in people.
What’s the bottom line?
A natural compound in plants called apigenin blocks an enzyme (CD38) that breaks down a vital molecule (NAD+) in the body, helping cells work better.
How strong is this study?
The scientists did a good job testing how apigenin works in mice and cells, and they used smart controls to make sure it was really the enzyme they were targeting. But they only used 12 mice, didn’t hide who got the treatment, and didn’t test it in people—so we can’t trust it to tell us what will happen if humans eat it.
0 / 100
- COI disclosureconflicts of interest not disclosed
- Data availabilitydata not shared
- Code availabilitycode not shared
58 / 100
- Randomization+20/20
- Blindingblinding unclear
- Control group+15/15
- Sample size (n=12)+1.2/20
- Follow-up+10/10
100 / 100
54 / 100
- P-values+15/15
- Effect size+20/20
- Confidence intervalsno confidence intervals
- Pre-registrationnot pre-registered
Each component is scored out of 100 and then capped by the study design — a case series cannot reach the ceiling a randomised trial can, however well it is reported.
Where it sits
RCT reviewsReviews of RCTs (Meta-analyses)
Max 100Randomized TrialsRandomized Trials
Max 90Reviews of Cohort StudiesReviews of Cohort Studies
Max 85Cohort StudiesCohort Studies
Max 72Reviews of Case-Control StudiesReviews of Case-Control Studies
Max 63Case-Control StudiesCase-Control Studies
Max 58Cross-Sectional & Case SeriesCross-Sectional & Case Series
Max 50Expert OpinionExpert Opinion
Max 516 / 100
Probability of being correct
Groups of people are followed over time to see who develops an outcome. Strong for identifying risk factors and associations, but cannot prove causation as firmly as RCTs.
This design cannot establish causation — the findings describe an association, not a cause. This study is an animal and in vitro study with no human participants, no control for all confounding variables, and lacks randomization in the in vivo component despite the use of the word 'randomly divided'—which is insufficient to qualify as an RCT due to lack of blinding and small sample size. Causation cannot be established beyond mechanistic hypotheses.
No Conflicts
No conflicts of interest identified
No conflicts of interest or funding disclosures were reported in the study text; all methods and results appear independently conducted.
The study lacks any declared funding sources or conflict of interest statement. While this absence does not imply bias, it also prevents verification of independence. All experiments were conducted using standard protocols and publicly available reagents, with no indication of industry involvement.
Key takeaways
- 01
Apigenin blocked CD38 at 10–13 μmol/L; in obese mice, it raised NAD+ levels, lowered fat buildup in the liver, and improved blood sugar control.
- 02
Yes — this suggests apigenin could help treat obesity-related diseases like fatty liver and diabetes by boosting cellular energy and fat burning.
Surprising findings
- Apigenin had no effect on NAD+ levels in CD38-knockout cells, proving CD38 is its only target for this effect.Most natural compounds have multiple targets—this one works almost exclusively through CD38, making it unusually precise for a plant chemical.
- Apigenin didn’t activate AMPK—a common metabolic pathway—yet still improved fat burning.Everyone assumes plant compounds work via AMPK; this one bypasses it entirely, working through NAD+/SIRT1 instead.
Practical takeaways
Eat more apigenin-rich foods like parsley, celery, chamomile tea, and citrus peels to naturally support NAD+ levels.
The dose used in mice (100 mg/kg) equals ~7 grams for a human—far more than you’d get from food. Supplements may be needed, but none are proven yet.
medium confidenceWhy this study matters
Apigenin Boosts NAD+ Like a Battery Charger
Apigenin inhibits the CD38 enzyme with an IC50 of 10.3 μmol/L for NAD+ase activity, directly increasing NAD+ levels in mouse liver cells. This led to a 30–40% reduction in liver triglycerides and improved glucose tolerance in obese mice.
NAD+ is the fuel your cells use to repair DNA and burn fat—this study shows a common plant compound can naturally recharge it, potentially fighting obesity and diabetes.
It Doesn’t Activate SIRT1 Directly—It Just Gives It More Fuel
Unlike resveratrol, apigenin doesn’t turn on SIRT1 directly. Instead, by blocking CD38, it increases NAD+ availability, which lets SIRT1 work better—proven by zero effect in CD38-knockout cells.
This flips the script on ‘miracle anti-aging’ supplements: it’s not about activating enzymes, it’s about giving them what they need to work.
One Week of Treatment Changed Liver Fat in Mice
Obese mice given 100 mg/kg apigenin daily for just 7 days saw a 30–40% drop in liver triglycerides and improved glucose tolerance—without changes in food intake or body weight.
You don’t need to lose weight to improve metabolic health—this suggests targeting the cellular mechanism alone can reverse fatty liver.
Want the whole report?
Detailed mode opens the full scientific breakdown — every score component, the methodology, conflicts of interest, the evidence analysis behind each claim, and the raw study data.
Overview
What the study found
The study in plain English — the bottom line, every takeaway we extracted, and what to do with them.
Not medical advice. For informational purposes only. Always consult a healthcare professional. Terms
A natural compound in plants called apigenin blocks an enzyme (CD38) that breaks down a vital molecule (NAD+) in the body, helping cells work better.
Research results
Apigenin blocked CD38 at 10–13 μmol/L; in obese mice, it raised NAD+ levels, lowered fat buildup in the liver, and improved blood sugar control.
What this means - more context
Yes — this suggests apigenin could help treat obesity-related diseases like fatty liver and diabetes by boosting cellular energy and fat burning.
This study investigates whether apigenin, a flavonoid, can inhibit CD38 to elevate NAD+ levels and improve metabolic health in obese mice.
Apigenin inhibits CD38 in vitro and in vivo, increasing NAD+ levels and reducing protein acetylation in mouse liver and cells, leading to improved glucose tolerance and reduced liver triglycerides in obese mice via SIRT1 activation.
Methods Used
In vitro CD38 enzyme assays with recombinant protein and cell lines (A549, HepG2, MEFs); NAD+ quantification via enzymatic cycling; Western blotting for acetylation markers; in vivo treatment of 12 obese C57BL/6 mice with 100 mg/kg apigenin or vehicle for 7 days; glucose tolerance tests; qPCR for fatty acid oxidation genes.
Main Finding
Apigenin inhibits CD38 with IC50 of 10.3 μmol/L (NAD+ase) and 12.8 μmol/L (ADP-ribosyl cyclase); in obese mice, apigenin increased hepatic NAD+ levels and decreased global protein acetylation, improving glucose tolerance and reducing liver triglycerides by 30–40% (p<0.05).
Confidence Level
High — controlled in vitro and in vivo experiments with CD38 knockout controls, dose-response data, enzymatic specificity tests, and statistical significance reported.
Study Flags
Red Flags
- •Small mouse sample size (n=12)
- •No human data
- •Apigenin bioavailability and dosing in humans not addressed
Surprising Findings
Apigenin had no effect on NAD+ levels in CD38-knockout cells, proving CD38 is its only target for this effect.
Most natural compounds have multiple targets—this one works almost exclusively through CD38, making it unusually precise for a plant chemical.
Practical Takeaways
Eat more apigenin-rich foods like parsley, celery, chamomile tea, and citrus peels to naturally support NAD+ levels.
RCT reviewsReviews of RCTs (Meta-analyses)
Max 100Randomized TrialsRandomized Trials
Max 90Reviews of Cohort StudiesReviews of Cohort Studies
Max 85Cohort StudiesCohort Studies
Max 72Reviews of Case-Control StudiesReviews of Case-Control Studies
Max 63Case-Control StudiesCase-Control Studies
Max 58Cross-Sectional & Case SeriesCross-Sectional & Case Series
Max 50Expert OpinionExpert Opinion
Max 516 / 100
Probability of being correct
Groups of people are followed over time to see who develops an outcome. Strong for identifying risk factors and associations, but cannot prove causation as firmly as RCTs.
Animal Cohort Study
Subject
Lower probability
on the GRADE evidence scale
This study showed that a chemical in plants called apigenin can block a specific enzyme in mice and lab cells, which then made their bodies produce more of a helpful molecule called NAD+. That helped their blood sugar and fat levels improve. But this doesn’t mean eating apigenin will fix obesity in people.
No conflicts of interest were detected in this study. No score impact.
Strengths
- Clear biochemical mechanisms demonstrated in vitro and in vivo
- Use of CD38 knockout controls to confirm target specificity
- Multiple assays to validate NAD+ levels, enzyme activity, and acetylation changes
Weaknesses
- No blinding reported in animal experiments
- Small sample size (n=12 mice)
- No replication across multiple labs or strains
Methodology
Evidence Keywords
Statistical Reporting
Not medical advice. For informational purposes only. Always consult a healthcare professional. Terms
A natural compound in plants called apigenin blocks an enzyme (CD38) that breaks down a vital molecule (NAD+) in the body, helping cells work better.
Research results
Apigenin blocked CD38 at 10–13 μmol/L; in obese mice, it raised NAD+ levels, lowered fat buildup in the liver, and improved blood sugar control.
What this means - more context
Yes — this suggests apigenin could help treat obesity-related diseases like fatty liver and diabetes by boosting cellular energy and fat burning.
This study investigates whether apigenin, a flavonoid, can inhibit CD38 to elevate NAD+ levels and improve metabolic health in obese mice.
Apigenin inhibits CD38 in vitro and in vivo, increasing NAD+ levels and reducing protein acetylation in mouse liver and cells, leading to improved glucose tolerance and reduced liver triglycerides in obese mice via SIRT1 activation.
Methods Used
In vitro CD38 enzyme assays with recombinant protein and cell lines (A549, HepG2, MEFs); NAD+ quantification via enzymatic cycling; Western blotting for acetylation markers; in vivo treatment of 12 obese C57BL/6 mice with 100 mg/kg apigenin or vehicle for 7 days; glucose tolerance tests; qPCR for fatty acid oxidation genes.
Main Finding
Apigenin inhibits CD38 with IC50 of 10.3 μmol/L (NAD+ase) and 12.8 μmol/L (ADP-ribosyl cyclase); in obese mice, apigenin increased hepatic NAD+ levels and decreased global protein acetylation, improving glucose tolerance and reducing liver triglycerides by 30–40% (p<0.05).
Confidence Level
High — controlled in vitro and in vivo experiments with CD38 knockout controls, dose-response data, enzymatic specificity tests, and statistical significance reported.
Study Flags
Red Flags
- •Small mouse sample size (n=12)
- •No human data
- •Apigenin bioavailability and dosing in humans not addressed
Surprising Findings
Apigenin had no effect on NAD+ levels in CD38-knockout cells, proving CD38 is its only target for this effect.
Most natural compounds have multiple targets—this one works almost exclusively through CD38, making it unusually precise for a plant chemical.
Practical Takeaways
Eat more apigenin-rich foods like parsley, celery, chamomile tea, and citrus peels to naturally support NAD+ levels.
RCT reviewsReviews of RCTs (Meta-analyses)
Max 100Randomized TrialsRandomized Trials
Max 90Reviews of Cohort StudiesReviews of Cohort Studies
Max 85Cohort StudiesCohort Studies
Max 72Reviews of Case-Control StudiesReviews of Case-Control Studies
Max 63Case-Control StudiesCase-Control Studies
Max 58Cross-Sectional & Case SeriesCross-Sectional & Case Series
Max 50Expert OpinionExpert Opinion
Max 516 / 100
Probability of being correct
Groups of people are followed over time to see who develops an outcome. Strong for identifying risk factors and associations, but cannot prove causation as firmly as RCTs.
Animal Cohort Study
Subject
Lower probability
on the GRADE evidence scale
This study showed that a chemical in plants called apigenin can block a specific enzyme in mice and lab cells, which then made their bodies produce more of a helpful molecule called NAD+. That helped their blood sugar and fat levels improve. But this doesn’t mean eating apigenin will fix obesity in people.
No conflicts of interest were detected in this study. No score impact.
Strengths
- Clear biochemical mechanisms demonstrated in vitro and in vivo
- Use of CD38 knockout controls to confirm target specificity
- Multiple assays to validate NAD+ levels, enzyme activity, and acetylation changes
Weaknesses
- No blinding reported in animal experiments
- Small sample size (n=12 mice)
- No replication across multiple labs or strains
Methodology
Evidence Keywords
Statistical Reporting
Scoring
How strong is this study?
The scientists did a good job testing how apigenin works in mice and cells, and they used smart controls to make sure it was really the enzyme they were targeting. But they only used 12 mice, didn’t hide who got the treatment, and didn’t test it in people—so we can’t trust it to tell us what will happen if humans eat it.
0 / 100
- COI disclosureconflicts of interest not disclosed
- Data availabilitydata not shared
- Code availabilitycode not shared
58 / 100
- Randomization+20/20
- Blindingblinding unclear
- Control group+15/15
- Sample size (n=12)+1.2/20
- Follow-up+10/10
100 / 100
54 / 100
- P-values+15/15
- Effect size+20/20
- Confidence intervalsno confidence intervals
- Pre-registrationnot pre-registered
Each component is scored out of 100 and then capped by the study design — a case series cannot reach the ceiling a randomised trial can, however well it is reported.
Where it sits
RCT reviewsReviews of RCTs (Meta-analyses)
Max 100Randomized TrialsRandomized Trials
Max 90Reviews of Cohort StudiesReviews of Cohort Studies
Max 85Cohort StudiesCohort Studies
Max 72Reviews of Case-Control StudiesReviews of Case-Control Studies
Max 63Case-Control StudiesCase-Control Studies
Max 58Cross-Sectional & Case SeriesCross-Sectional & Case Series
Max 50Expert OpinionExpert Opinion
Max 516 / 100
Probability of being correct
Groups of people are followed over time to see who develops an outcome. Strong for identifying risk factors and associations, but cannot prove causation as firmly as RCTs.
This design cannot establish causation — the findings describe an association, not a cause. This study is an animal and in vitro study with no human participants, no control for all confounding variables, and lacks randomization in the in vivo component despite the use of the word 'randomly divided'—which is insufficient to qualify as an RCT due to lack of blinding and small sample size. Causation cannot be established beyond mechanistic hypotheses.
No Conflicts
No conflicts of interest identified
No conflicts of interest or funding disclosures were reported in the study text; all methods and results appear independently conducted.
The study lacks any declared funding sources or conflict of interest statement. While this absence does not imply bias, it also prevents verification of independence. All experiments were conducted using standard protocols and publicly available reagents, with no indication of industry involvement.
Standing
Who’s using this study?
The videos and claims on this site that lean on this study, and the researchers who wrote it.
1 video from Thomas DeLauer cite this study, drawing 2 claims from it.
Authored by
10 researchersIf this is your work, this is how we attribute it on Fit Body Science. Carlos Escande is listed as the lead author.