The Study
Impaired ketogenesis and increased acetyl-CoA oxidation promote hyperglycemia in human fatty liver.
We don't know what kind of study this was—was it watching people, or giving them treatments? Without knowing that, we can't say if fatty liver causes high blood sugar or if they just happen together. It's like seeing clouds and rain and guessing which came first—you just don't know.
Analysis score
Maximum 90 for a randomized controlled trial.
Where the score came from
When your liver gets fatty, it stops making ketones (a fuel for your brain) and instead burns fat to make energy inside the liver, which accidentally makes too much sugar.
Where does this study sit?
Reviews of RCTs (Meta-analyses)
Max 100Randomized Trials
Max 90Reviews of Cohort Studies
Max 85Cohort Studies
Max 72Reviews of Case-Control Studies
Max 63Case-Control Studies
Max 58Cross-Sectional & Case Series
Max 50Expert Opinion
Max 560 / 100
Quality score
Participants are randomly assigned to treatment or control groups, minimizing bias. The gold standard for testing whether an intervention causes an effect.
Key takeaways
Summary
Based on the study abstract and findings.
- 1This means your liver is wasting energy making sugar instead of sending ketones to your brain — which may explain why people with fatty liver often have high blood sugar even when fasting.
- 2People with fatty liver made 30% less BHB (a ketone) during fasting, but their liver burned 57% more fat in the TCA cycle, used 30% more oxygen per fat molecule, and made 30% more glucose than healthy people.
Score breakdown, methodology, conflicts of interest, evidence analysis & raw study data
Publication
Journal
JCI insight
Year
2019
Authors
J. Fletcher, S. Deja, S. Satapati, Xiaorong Fu, Shawn C. Burgess, J. Browning
Related Content
Claims (6)
When carbohydrate intake is low, the liver breaks down fatty acids to produce ketone bodies.
In people with nonalcoholic fatty liver disease, the liver uses more oxygen while fasting, and this increased energy use is linked to higher glucose production, which raises blood sugar levels.
In people with nonalcoholic fatty liver disease, the liver produces the same amount of acetyl-CoA from fat breakdown as in healthy people, but it uses that acetyl-CoA differently—burning it in the TCA cycle instead of making ketones, which increases oxygen use and glucose production.
In people with fatty liver and moderate to high liver fat, a 24-hour fast leads to reduced ketone production, which coincides with increased use of acetyl-CoA in the energy cycle, higher oxygen use in the liver, and greater glucose production and blood sugar levels, showing that how acetyl-CoA is directed within liver cells—not how much is made—causes elevated blood glucose.
During a 24-hour fast, people with nonalcoholic fatty liver disease produce less β-hydroxybutyrate than healthy individuals, and this lower production is linked to higher fat levels in the liver; acetoacetate production does not change.
In people with nonalcoholic fatty liver disease, the biochemical process that converts acetoacetate into β-hydroxybutyrate is reduced, suggesting an impairment in mitochondrial energy metabolism or the enzyme responsible for this conversion.
Not medical advice. For informational purposes only. Always consult a qualified healthcare professional before making health decisions.