When the Cav3.1 gene is removed from neurons in the hypothalamus, the normal reduction in food intake triggered by a high-protein diet no longer occurs.
Mechanism
Synthesis from 1 study
When you eat high-protein food, leucine enters brain cells that control hunger and turns on a calcium channel called Cav3.1. This triggers those cells to signal the brain to stop eating. If the Cav3.1 channel is missing, the brain doesn't get the signal to stop, so eating doesn't decrease even with...
Most probable mechanism
When dietary protein is digested, the amino acid leucine enters the brain and binds to Cav3.1 calcium channels in specific hunger-regulating neurons. This binding makes the channels open more easily when the neurons are electrically stimulated, allowing calcium to flow into the cells. The calcium surge activates these neurons, 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 channels open and permit calcium influx into hypothalamic POMC neurons
Calcium influx activates POMC neurons, triggering downstream anorectic signaling pathways
Activated POMC neurons suppress food intake and promote weight loss through central satiety circuits
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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