The Claim
Endothelin-1 inhibits insulin-stimulated glucose uptake in isolated rat adipocytes without altering insulin binding, indicating a post-receptor mechanism of interference with insulin action in adipose tissue.
What the research says
Roughly balanced
Support and challenge are close. The picture may shift as more studies come in.
These are independent scores, not a percentage. Higher-grade studies count more, so a single strong opposing study can outweigh several weaker ones.
Endothelin-1 reduces the ability of insulin to promote glucose uptake in fat cells from rats, even though it does not affect how insulin binds to its receptor, meaning the interference occurs after insulin binds.
See the scientific wording
Endothelin-1 inhibits insulin-stimulated glucose uptake in isolated rat adipocytes without altering insulin binding, suggesting a post-receptor mechanism of interference with insulin action in adipose tissue.
A signaling molecule called endothelin-1 attaches to fat cells and triggers an internal chain of events that stops insulin from moving glucose transporters to the cell surface, so glucose cannot enter the cell even though insulin binds normally.
What the research says
1 studyStudy: Endothelin-1 inhibits insulin-stimulated glucose uptake in isolated rat adipocytes.
In fat cells from rats, a molecule called endothelin-1 blocks insulin from helping the cell take in sugar, even though insulin can still attach to the cell normally—meaning the problem happens after insulin sticks on, not before.
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.