Loss of BCATm correlates with a loss in BCKD-stimulated insulin secretion, but has not been associated with losses in insulin secretion from other metabolic pathways. BCATc regulates the mTORC1 signaling and TCR-induced glycolytic metabolism pathways during CD4+ T cell activation. In the brain, BCATc regulates the amount of glutamate production for use as a neurotransmitter or for future γ-Aminobutyric acid (GABA) synthesis.
BCATm loss is associated with decreased insulin secretion triggered by BCKD, but it has not been linked to declines in insulin secretion from other metabolic pathways. BCATc plays a role in regulating mTORC1 signaling and glycolytic metabolism during T cell activation, and in the brain, it influences glutamate production for neurotransmitter or GABA synthesis.