Expression of glucokinase (GCK) in the dorsal vagal complex was significantly reduced in diabetic mice.
Molecular expression of KATP channel components was unchanged.
Synaptic responses of NTS neurons to GCK inhibition were significantly altered.
Effects of increased [glucose] on action potential firing was attenuated.
Reduced GCK-dependent, glucose-mediated responses in the NTS likely contribute to autonomic dysregulation in diabetes.