The Study
Prostaglandin E2-EP4 Axis Promotes Lipolysis and Fibrosis in Adipose Tissue Leading to Ectopic Fat Deposition and Insulin Resistance.
This study looked at people with and without certain fat problems and noticed a possible link to a body signal called PGE2-EP4. But it didn't prove that this signal causes the problem—it just found that they sometimes happen together.
Analysis score
Maximum 58 for a case-control study.
Where the score came from
When you eat, your body releases insulin, which triggers a chemical signal (PGE2) that keeps fat breaking down even when you're not fasting. This keeps going too long in very obese people, causing fat to build up in the wrong places and leading to diabetes. But in some obese people, this signal is broken — and they stay healthy.
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 520 / 100
Quality score
Researchers compare people who have a condition (cases) with similar people who do not (controls), looking back in time for differences in exposure. Useful but more prone to bias.
Key takeaways
Summary
Based on the study abstract and findings.
- 1Yes — if this signal is disrupted, obese individuals may avoid insulin resistance and related diseases despite having excess fat.
- 2Not specified
Score breakdown, methodology, conflicts of interest, evidence analysis & raw study data
Publication
Journal
Cell reports
Year
2020
Authors
Tomoaki Inazumi, Kiyotaka Yamada, Naritoshi Shirata, Hiroyasu Sato, Y. Taketomi, Kazunori Morita, H. Hohjoh, Soken Tsuchiya, K. Oniki, Takehisa Watanabe, Yutaka Sasaki, Y. Oike, Y. Ogata, J. Saruwatari, M. Murakami, Y. Sugimoto
Related Content
Claims (4)
When no food is consumed during fasting, insulin levels drop, leading to the breakdown of fat stores and increased burning of fat in the liver.
In people with morbid obesity, prostaglandin E2 acting on the EP4 receptor in fat cells maintains a baseline level of fat breakdown during normal eating and fasting cycles, which contributes to tissue scarring, fat accumulation in organs, and reduced insulin sensitivity.
During feeding, insulin triggers the production of prostaglandin E2 in fat cells, and this process maintains a baseline level of fat breakdown as a regulatory response.
Changes in the PGE2-EP4 signaling pathway occur alongside a condition in which individuals have excess body fat but do not show typical metabolic problems like insulin resistance or high blood pressure.
Not medical advice. For informational purposes only. Always consult a qualified healthcare professional before making health decisions.