Cited by 746Diabetes Treatment and ManagementPancreatic function and diabetesNeuropeptides and Animal Physiology

GIP and GLP-1, the two incretin hormones: Similarities and differences

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Seino, Yutaka, Fukushima, Mitsuo, Yabe, Daisuke·2010·Journal of Diabetes Investigation

Abstract

Gastric inhibitory polypeptide (GIP) and glucagon‐like peptide‐1 (GLP‐1) are the two primary incretin hormones secreted from the intestine on ingestion of glucose or nutrients to stimulate insulin secretion from pancreatic β cells. GIP and GLP‐1 exert their effects by binding to their specific receptors, the GIP receptor (GIPR) and the GLP‐1 receptor (GLP‐1R), which belong to the G‐protein coupled receptor family. Receptor binding activates and increases the level of intracellular cyclic adenosine monophosphate in pancreatic β cells, thereby stimulating insulin secretion glucose‐dependently. In addition to their insulinotropic effects, GIP and GLP‐1 play critical roles in various biological processes in different tissues and organs that express GIPR and GLP‐1R, including the pancreas, fat, bone and the brain. Within the pancreas, GIP and GLP‐1 together promote β cell proliferation and inhibit apoptosis, thereby expanding pancreatic β cell mass, while GIP enhances postprandial glucagon response and GLP‐1 suppresses it. In adipose tissues, GIP but not GLP‐1 facilitates fat deposition. In bone, GIP promotes bone formation while GLP‐1 inhibits bone absorption. In the brain, both GIP and GLP‐1 are thought to be involved in memory formation as well as the control of appetite. In addition to these differences, secretion of GIP and GLP‐1 and their insulinotropic effects on β cells have been shown to differ in patients with type 2 diabetes compared to healthy subjects. We summarize here the similarities and differences of these two incretin hormones in secretion and metabolism, their insulinotropic action on pancreatic β cells, and their non‐insulinotropic effects, and discuss their potential in treatment of type 2 diabetes. (J Diabetes Invest, doi: 10.1111/j.2040‐1124.2010.00022.x, 2010)

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Authors
Seino, Y., Fukushima, M., & Yabe, D.
Affiliations
  • Kansai Electric Power (Japan) (JP)
  • Okayama Prefectural University (JP)
Corresponding author
Seino, Yutaka
Venue
Journal of Diabetes Investigation
Publisher
Wiley
Published
2010-02
Volume
1
Issue
1-2
Pages
8-23
ISSN
  • 2040-1116 (ISSN-L)
  • 2040-1124
OpenAlex
W1582261481
Cited by
746
References
184
Citations by year
2026: 68 · 2025: 94 · 2024: 92 · 2023: 64 · 2022: 59 · 2021: 61 · 2020: 42 · 2019: 59 · 2018: 34 · 2017: 30 · 2016: 32 · 2015: 25 · 2014: 25 · 2013: 18 · 2012: 20
FWCI
2.77
Type
journal article
Language
en
Open access
Locations
  • Journal of Diabetes Investigation (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
Keywords
glucose-dependent insulinotropic polypeptide, glucagon-like peptide-1, incretins, GIP receptor, GLP-1 receptor, G protein-coupled receptors, insulin secretion, pancreatic beta cells, beta-cell proliferation, glucagon, adipose tissue, bone metabolism, brain, memory, appetite regulation, type 2 diabetes, incretin-based therapy

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