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The study aimed to determine the role of brain glucagon action in regulating hepatic glucose production (HGP). It infused glucagon into the carotid and vertebral arteries and a peripheral vein to increase glucagon in the brain and the liver, respectively. Results showed that increased brain glucagon signaling reduced circulating free fatty acids and glycerol but did not reduce HGP. The liver's autoregulation prevented a change in HGP. The study concludes that while brain glucagon can alter hepatic carbon flux, it does not appear to be responsible for the transient fall in HGP following a rise in glucagon.
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