Changing a specific part of the Cav3.1 protein prevents it from sending signals that tell the body it is full after eating protein.
Mechanism
Synthesis from 1 study
Leucine from protein binds to Cav3.1 in brain cells that control fullness, making them more likely to activate. This triggers a calcium signal that tells the brain to stop eating. Without this binding site, the brain cannot detect protein intake and does not signal fullness.
Most probable mechanism
When dietary protein breaks down into leucine, leucine binds to a specific site on the Cav3.1 protein in brain cells that control fullness. This binding makes the Cav3.1 channel open more easily, letting calcium flow into the cells. The calcium surge activates these cells, which send signals to stop eating and reduce food intake.
Leucine from dietary protein binds to a hydrophobic pocket in the Cav3.1 voltage-gated calcium channel
Leucine binding lowers the voltage threshold required for Cav3.1 channel opening
Cav3.1 channel opening permits calcium influx into hypothalamic POMC neurons
Calcium influx activates POMC neurons, triggering downstream anorectic signaling pathways
Activated POMC neurons suppress appetite and reduce food intake
Evidence from Studies
Supporting (1)
Community contributions welcome
Cav3.1 is a neuronal leucine sensor that mediates satiety and weight loss in response to dietary protein
Contradicting (0)
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