Duodenal GLP-1 signaling regulates hepatic glucose production through a PKC-δ-dependent neurocircuitry

Cell Death Dis. 2017 Feb 9;8(2):e2609. doi: 10.1038/cddis.2017.28.

Abstract

Intestinal glucagon-like peptide-1 (GLP-1) is a hormone that stimulates insulin secretion and acts as a neuropeptide to control glucose homeostasis, but little is known whether intestinal GLP-1 has any effect in the control of hepatic glucose production (HGP). Here we found that intraduodenal infusion of GLP-1 activated duodenal PKC-δ, lowered HGP and was accompanied by a decrease in hepatic expression of gluconeogenic enzymes and an increase in hepatic insulin signaling in rats. However, gut co-infusion of either the GLP-1 receptor antagonist Ex-9, or the PKC-δ inhibitor rottlerin with GLP-1, negated the ability of gut GLP-1 to lower HGP and to increase hepatic insulin signaling during clamps. The metabolic and molecular signal effects of duodenal GLP-1 were also negated by co-infusion with tetracaine, pharmacologic inhibition of N-methyl-d-aspartate receptors within the dorsalvagal complex, or hepatic vagotomy in rats. In summary, we identified a neural glucoregulatory function of gut GLP-1 signaling.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Duodenum / metabolism*
  • Glucagon-Like Peptide 1 / metabolism*
  • Glucagon-Like Peptide-1 Receptor / metabolism
  • Glucose / metabolism*
  • Homeostasis / physiology
  • Insulin / metabolism
  • Liver / metabolism*
  • Protein Kinase C-delta / metabolism*
  • Rats
  • Receptors, N-Methyl-D-Aspartate / metabolism
  • Signal Transduction / physiology*

Substances

  • Glucagon-Like Peptide-1 Receptor
  • Insulin
  • Receptors, N-Methyl-D-Aspartate
  • Glucagon-Like Peptide 1
  • Protein Kinase C-delta
  • Glucose