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. 2013 Jun 14;62(7):2295–2307. doi: 10.2337/db12-1629

FIG. 7.

FIG. 7.

Model for the mechanism of regulation of glucose metabolism in muscle and liver by leptin in the VMH. Ob-Rb in the VMH plays a key role in the regulation of glucose metabolism and insulin sensitivity in muscle and liver by leptin. Leptin-activated MEK-ERK signaling in the VMH increases insulin sensitivity and glucose utilization in red muscle through activation of MCR in the VMH. Ob-Rb–expressing VMH neurons likely activate POMC neurons either in the ARC itself (14) or at their synaptic connections with VMH neurons through the MEK-ERK pathway. The MEK-ERK pathway then stimulates synaptic plasticity for POMC neurons and MCR-expressing neurons in the VMH. Whereas other brain sites may contribute to the leptin-induced enhancement of the suppressive effect of insulin on hepatic glucose production, leptin-activated STAT3 signaling in the VMH mediates this enhancement by inhibiting glycogen phosphorylase a activity in liver. 3V, third ventricle.