Department of Medicine, Division of Endocrinology and Diabetes, and Department of Molecular Pharmacology, Albert Einstein College of Medicine, Bronx, New York, USA.
Address correspondence to: Allen M. Spiegel, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Belfer 312, Bronx, New York 10461, USA. Phone: 718.430.2801; Email: firstname.lastname@example.org.
First published January 16, 2018 - More info
Hepatic glucose production (HGP) is a key determinant of glucose homeostasis. Glucagon binding to its cognate seven-transmembrane Gs-coupled receptor in hepatocytes stimulates cAMP production, resulting in increased HGP. In this issue of the JCI, Rossi and colleagues tested the hypothesis that activation of hepatic Gi–coupled receptors, which should inhibit cAMP production, would oppose the cAMP-inducing action of glucagon and thereby decrease HGP. Surprisingly, however, the opposite occurred: activation of Gi signaling increased HGP via a novel mechanism, while inhibition of Gi signaling reduced HGP. These results define a new physiologic role for hepatic Gi signaling and identify a potential therapeutic target for HGP regulation.
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