GIP and GLP-1, the two incretin hormones: Similarities and differences
Open accessAbstract
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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GIP is produced by intestinal endocrine K cells and, like GLP-1, stimulates insulin secretion from pancreatic β cells in a glucose-dependent manner.
“Intestinal endocrine K cells produce gastric inhibitory polypeptide (GIP). Like GLP-1, GIP stimulates insulin secretion from pancreatic β cells in a glucose-dependent manner (124).”
From GLP−1 receptor agonists for the treatment of obesity: Role as a promising approach (2023) · cites this paper as [124]
GIP analogues were initially not a desirable field of research for T2D treatment because GIP action was thought to be lost in T2D and GIP can augment glucagon secretion.
“The development of GIP analogues for T2D treatment was initially not a desirable field of research due to GIP action being thought to be lost in T2D and GIPs ability to augment glucagon secretion.3,261”
From A review of current trends with type 2 diabetes epidemiology, aetiology, pathogenesis, treatments and future perspectives (2021) · cites this paper as [261]
GLP-1 analogues are effective insulinotropic agents and successfully suppress glucagon secretion in a glucose-dependent manner.
“These GLP-1 analogues are effective insulinotropic agents and successfully suppress glucagon secretion in a glucose-dependent manner.260–261”
From A review of current trends with type 2 diabetes epidemiology, aetiology, pathogenesis, treatments and future perspectives (2021) · cites this paper as [261]
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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
- PMC
- PMC4020673
- 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
- bronze
- doi.org
- 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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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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