The Claim
Insulin activates the prostaglandin E2 synthesis pathway in adipocytes during feeding, and this activation sustains basal lipolysis as a negative feedback mechanism.
What the research says
Supports is higher
Support is ahead, but a single strong opposing study can change this.
These are independent scores, not a percentage. Higher-grade studies count more, so a single strong opposing study can outweigh several weaker ones.
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.
See the scientific wording
Insulin activates the prostaglandin E2 synthesis pathway in adipocytes during feeding, which in turn sustains basal lipolysis as a negative feedback mechanism.
When you eat, insulin tells fat cells to stop breaking down fat, but it also triggers them to make a chemical that reactivates a small amount of fat breakdown. This chemical binds to a receptor on the fat cell, keeping fat breakdown going just enough to prevent too much fat storage. If this happens too much over time, the fat tissue becomes stiff and can't expand, forcing fat to build up in other organs like the liver and muscles.
What the research says
1 studyWhen you eat and your insulin goes up, your fat cells make a chemical called PGE2 that keeps breaking down a little bit of fat—even though insulin usually tells fat cells to store fat. This might help balance energy use.
Score breakdown, mechanism chain, raw evidence, ideal studies needed & 1 supporting studies
Not medical advice. For informational purposes only. Always consult a qualified healthcare professional before making health decisions.