The Claim
Thyroid hormone increases phosphorylation of acetyl-CoA carboxylase (ACC) through activation of AMPK in multiple human and mouse cell lines, resulting in reduced malonyl-CoA levels and increased fatty acid entry into mitochondria for oxidation.
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.
Thyroid hormone triggers a biochemical chain reaction in human and mouse cells that reduces malonyl-CoA and allows more fatty acids to enter mitochondria to be burned for energy.
See the scientific wording
Thyroid hormone increases phosphorylation of acetyl-CoA carboxylase (ACC) via AMPK activation in multiple human and mouse cell lines, which reduces malonyl-CoA levels and promotes fatty acid entry into mitochondria for oxidation.
Thyroid hormone triggers a surge of calcium inside cells, which turns on a kinase called CaMKKβ. This kinase activates AMPK, which then modifies acetyl-CoA carboxylase to stop it from making malonyl-CoA. With less malonyl-CoA, fatty acids can enter mitochondria and be burned for energy.
What the research says
1 studyThyroid hormone turns on a cellular switch (AMPK) that tells the cell to stop blocking fat from entering the energy-producing parts, so more fat gets burned for energy.
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.