L-leucine reduces activity in specific brain neurons by blocking a type of calcium flow that depends on SERCA ATPase and 2-APB, and this mechanism is different from the calcium pathway that normally...
Mechanism
Synthesis from 1 study
L-leucine turns off hunger signals in the brain by keeping calcium inside storage compartments, which shuts down a calcium entry channel. Less calcium enters the cell, making it less active and reducing signals that drive eating.
Most probable mechanism
L-leucine reduces calcium flow into certain brain cells by blocking a calcium channel that depends on internal calcium stores. This happens because leucine helps keep those internal stores full, which turns off the channel that lets calcium in from outside. Less calcium inside the cell makes the cell less active, reducing signals that drive hunger.
Extracellular L-leucine modulates the activity of the sarco/endoplasmic reticulum Ca2+ ATPase (SERCA), enhancing calcium reuptake into the endoplasmic reticulum and stabilizing intracellular calcium stores.
Stabilized endoplasmic reticulum calcium stores suppress the opening of store-operated calcium (SOC) channels on the plasma membrane, reducing calcium influx from the extracellular space.
Reduced store-operated calcium influx lowers intracellular calcium concentration in NPY/AGRP neurons, leading to membrane hyperpolarization and decreased neuronal firing.
Decreased neuronal activity in NPY/AGRP neurons reduces the secretion of the orexigenic neuropeptide AGRP, suppressing downstream hunger signals.
Evidence from Studies
Supporting (1)
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Rapid sensing of l-leucine by human and murine hypothalamic neurons: Neurochemical and mechanistic insights
Contradicting (0)
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