Leucine, an amino acid from dietary protein, activates the Cav3.1 protein in hypothalamic neurons, which triggers signals that reduce hunger.
Mechanism
Synthesis from 1 study
Eating protein releases leucine, which locks into a special calcium channel in brain cells that control hunger. This makes the channel open more easily, letting calcium flow in and turn on those cells. Once activated, the cells send a signal to stop eating and burn fat.
Most probable mechanism
When you eat protein, the amino acid leucine enters the brain and binds to a specific calcium channel called Cav3.1 in appetite-regulating neurons. This binding makes the channel open more easily when the neuron is electrically active, allowing calcium to rush in. The calcium surge activates these neurons, which send signals to stop eating and reduce food intake.
Leucine 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 promote weight loss 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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