The Study
FTO is necessary for the induction of leptin resistance by high-fat feeding
This study looked at mice with a changed gene to see how they react to fatty food and a hormone called leptin. It found that mice without the gene didn't get as hungry after eating fatty food, but that doesn't mean the same thing happens in people. It's like noticing your pet dog acts differently when you feed it a new treat — it tells you something interesting, but not what will happen to humans.
Analysis score
Maximum 72 for a cohort study.
Where the score came from
This study found that mice without a gene called FTO keep feeling full after eating, even when they eat lots of fatty food and get obese.
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 516 / 100
Quality score
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.
Key takeaways
Summary
Based on the study abstract and findings.
- 1Yes — if this works in humans, blocking FTO could help obese people feel full and eat less, even if they're overweight.
- 2Mice without FTO ate 50% less food after a leptin shot, while normal mice ate the same amount.
- 3Their brains showed less inflammation (NF-κB activity) when on a high-fat diet.
Score breakdown, methodology, conflicts of interest, evidence analysis & raw study data
Publication
Journal
Molecular Metabolism
Year
2015
Authors
Y.C. Loraine Tung, P. Gulati, Che-Hsiung Liu, D. Rimmington, Rowena J. Dennis, Marcella K. Ma, V. Saudek, S. O’Rahilly, A. Coll, Giles S.H. Yeo
Related Content
Claims (6)
Higher consumption of dietary fat increases leptin signaling, resulting in lower food intake due to greater feelings of fullness.
In mice, a high-fat diet increases activity of inflammatory genes in the hypothalamus, and this increase is reduced in mice with less FTO gene function, with the effect proportional to how much FTO is missing.
In mice, the FTO protein binds to TRIP4 in brain cells that regulate appetite, and this binding is necessary to activate the NF-κB inflammatory pathway.
In mice, a genetic deficiency in the FTO gene blocks the loss of leptin sensitivity in the hypothalamus that normally occurs when eating a high-fat diet, even when body fat increases, by reducing activity in the NF-κB signaling pathway.
In mice fed a high-fat diet, those lacking the FTO gene eat 50% less food after receiving leptin than mice with the normal gene, while leptin does not reduce food intake in mice with the normal gene.
In mice lacking the FTO gene, directly activating the NF-κB signaling pathway in the hypothalamus through TNFα restores leptin resistance, indicating that this pathway can override the increased leptin sensitivity caused by FTO deficiency.
Not medical advice. For informational purposes only. Always consult a qualified healthcare professional before making health decisions.