The Study
Obesogenic memory can confer long-term increases in adipose tissue but not liver inflammation and insulin resistance after weight loss
This study watched people and mice before and after they lost weight, and noticed that in some people, their fat tissue stayed inflamed even after losing weight — but their liver got better. It doesn't prove that being overweight causes the fat tissue to stay inflamed, just that they often happen together.
Analysis score
Maximum 72 for a cohort study.
Where the score came from
Even after losing a lot of weight, some people’s fat tissue stays inflamed and resistant to insulin — like a stubborn memory of being obese — while the liver gets better.
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 563 / 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 — this means even after losing weight, some people still have hidden metabolic risks because their fat tissue doesn't fully recover, which could explain why they’re still at risk for diabetes or heart disease.
- 2In 42% of people who lost weight after bariatric surgery, fat tissue inflammation didn't improve, even though fat cells got smaller and blood sugar improved.
- 3In mice, weight regain happened because they ate more, not because they burned fewer calories.
Score breakdown, methodology, conflicts of interest, evidence analysis & raw study data
Publication
Journal
Molecular Metabolism
Year
2016
Authors
J. Schmitz, N. Evers, M. Awazawa, Hayley T. Nicholls, H. Brönneke, A. Dietrich, J. Mauer, M. Blüher, J. Brüning
Related Content
Claims (6)
Insulin resistance and chronic inflammation interact in a cycle that increases fat buildup in the liver.
After bariatric surgery and sustained weight loss, liver inflammation and blood sugar regulation improve in obese adults, but in about 42% of individuals, inflammation in fat tissue and insulin resistance in fat cells remain unchanged despite smaller fat cells and lower body weight.
When mice and humans lose weight, liver inflammation decreases and insulin sensitivity in the liver improves, but inflammation and insulin resistance in visceral fat tissue do not improve even when fat cells shrink and body weight returns to normal.
After losing weight, mice regain weight mainly because they eat more, not because they burn less energy; when their food intake is controlled to match that of mice that never lost weight, they do not regain weight.
After weight loss in mice, fat cells return to normal size, but immune cell presence and inflammation-related gene activity in visceral fat do not decrease.
After mice lose weight, their pancreatic beta cells stay enlarged and continue to release more insulin in response to glucose, even though the body's overall sensitivity to insulin has not returned to normal.
Not medical advice. For informational purposes only. Always consult a qualified healthcare professional before making health decisions.