Central regulation of glucose-dependent insulinotropic polypeptide secretion

Vitam Horm. 2010:84:185-201. doi: 10.1016/B978-0-12-381517-0.00006-0.

Abstract

Glucose-dependent insulinotropic peptide (GIP) and glucagon-like peptide-1 (GLP-1) are potent stimulators of glucose-dependent insulin secretion, a phenomenon known as incretin effect. After food ingestion, the circulating levels of GIP and GLP-1 rise more quickly than could be explained by the arrival of unabsorbed nutrients that have a direct stimulatory effect on K- and L-cells. Previous studies have thoroughly investigated the possible role of the autonomic nervous system on GIP secretion, demonstrating conflicting results. Recent data from intracerebroventricular infusions of different neuropeptides that participate in the overall regulation of energy homeostasis, suggest the possible existence of additional neuroendocrine mechanisms that may contribute to a central regulation of GIP secretion.

Publication types

  • Review

MeSH terms

  • Animals
  • Autonomic Nervous System / physiology*
  • Gastric Inhibitory Polypeptide / metabolism
  • Gastric Inhibitory Polypeptide / physiology*
  • Glucagon-Like Peptide 1 / metabolism
  • Glucagon-Like Peptide 1 / physiology
  • Humans
  • Insulin / metabolism
  • Insulin / physiology
  • Insulin Secretion
  • Mice
  • Parasympathetic Nervous System / physiology*

Substances

  • Insulin
  • Gastric Inhibitory Polypeptide
  • Glucagon-Like Peptide 1