In mice, removing the Cacna1g gene specifically from POMC neurons prevents high-protein diets from reducing food intake and body weight.
Mechanism
Synthesis from 1 study
High-protein diets raise leucine levels in the brain, which turn on specific calcium channels in appetite-controlling neurons. This triggers those neurons to signal fullness, reducing food intake and causing weight loss. Without these channels, the brain cannot detect the protein signal, so...
Most probable mechanism
When a high-protein diet increases leucine in the brain, leucine binds to Cav3.1 calcium channels on POMC neurons, making them easier to activate. This causes calcium to flow into the neurons, turning them on. These activated neurons send signals that stop hunger and reduce food intake, leading to weight loss.
Leucine from dietary protein binds to a hydrophobic pocket in the Cav3.1 voltage-gated calcium channel on POMC neurons
Leucine binding lowers the voltage threshold required for Cav3.1 channel opening
Cav3.1 channels open and allow calcium ions to enter POMC neurons
Calcium influx activates POMC neurons, triggering downstream anorectic signaling pathways
Activated POMC neurons suppress appetite and reduce body weight through central satiety circuits
Evidence from Studies
Supporting (1)
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Cav3.1 is a neuronal leucine sensor that mediates satiety and weight loss in response to dietary protein
Contradicting (0)
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