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
See the related article at Hepatic Gi signaling regulates whole-body glucose homeostasis.
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.
A subscription is required for you to read this article in full. If you are a subscriber, you may sign in to continue reading.
Click here to sign into your account.
Please select one of the subscription options, which includes a low-cost option just for this article.
If you are at an institution or library and believe you should have access, please check with your librarian or administrator (more information).
Please try these troubleshooting tips.