ROLE OF CENTRAL NEURAL MECHANISMS IN THE REGULATION OF HEPATIC GLUCOSE-METABOLISM

Central monoamine neurotransmitters affect blood glucose homeostasis. Activation of central cholinergic, noradrenergic histaminergic, and se rotonergic neurons rapidly increase hepatic glucose output via the sym pathetic nervous system. Acute hyperglycemia is mediated by three dist inct pathways: the action of epinephrine on the liver, the action of g lucagon on the liver, and the direct innervation of the liver. The rel ative contribution of these factors to hyperglycemia can be altered by diet and the kinds of neurotransmitters evoked in the central nervous system, but the magnitude of epinephrine secretion is closely related to the magnitude of hyperglycemia. On the other hand, neuropharmacolo gical stimulation of central cholinergic muscarinic receptors, histami nergic H-1 receptors, and serotonergic 5-HT2 receptors increases hypot halamic noradrenergic neuronal activity, which is associated with hype rglycemia. In contrast, central GABA(A) receptors play an inhibitory r ole in the regulation of hepatic glucose metabolism. Thus, central mon oaminergic neurons could be linked together, and play a homeostatic ro le in the regulation of hepatic glucose metabolism.