Glucose-dependent insulinotropic polypeptide (GIP)
(2025) In Molecular Metabolism 95.- Abstract
Background: Glucose-dependent insulinotropic polypeptide (GIP) was the first incretin identified and plays an essential role in the maintenance of glucose tolerance in healthy humans. Until recently GIP had not been developed as a therapeutic and thus has been overshadowed by the other incretin, glucagon-like peptide 1 (GLP-1), which is the basis for several successful drugs to treat diabetes and obesity. However, there has been a rekindling of interest in GIP biology in recent years, in great part due to pharmacology demonstrating that both GIPR agonism and antagonism may be beneficial in treating obesity and diabetes. This apparent paradox has reinvigorated the field, led to new lines of investigation, and deeper understanding of GIP.... (More)
Background: Glucose-dependent insulinotropic polypeptide (GIP) was the first incretin identified and plays an essential role in the maintenance of glucose tolerance in healthy humans. Until recently GIP had not been developed as a therapeutic and thus has been overshadowed by the other incretin, glucagon-like peptide 1 (GLP-1), which is the basis for several successful drugs to treat diabetes and obesity. However, there has been a rekindling of interest in GIP biology in recent years, in great part due to pharmacology demonstrating that both GIPR agonism and antagonism may be beneficial in treating obesity and diabetes. This apparent paradox has reinvigorated the field, led to new lines of investigation, and deeper understanding of GIP. Scope of Review: In this review, we provide a detailed overview on the multifaceted nature of GIP biology and discuss the therapeutic implications of GIPR signal modification on various diseases. Major Conclusions: Following its classification as an incretin hormone, GIP has emerged as a pleiotropic hormone with a variety of metabolic effects outside the endocrine pancreas. The numerous beneficial effects of GIPR signal modification render the peptide an interesting candidate for the development of pharmacotherapies to treat obesity, diabetes, drug-induced nausea and both bone and neurodegenerative disorders.
(Less)
- author
- organization
- publishing date
- 2025-05
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Diabetes, GIP, GLP-1, Incretin, Insulin, Obesity
- in
- Molecular Metabolism
- volume
- 95
- article number
- 102118
- publisher
- Elsevier
- external identifiers
-
- pmid:40024571
- scopus:86000367480
- ISSN
- 2212-8778
- DOI
- 10.1016/j.molmet.2025.102118
- language
- English
- LU publication?
- yes
- id
- 9c9042ec-24d1-4623-a5cb-3ea5e63989e0
- date added to LUP
- 2025-06-18 12:32:35
- date last changed
- 2025-07-16 15:32:35
@article{9c9042ec-24d1-4623-a5cb-3ea5e63989e0,
abstract = {{<p>Background: Glucose-dependent insulinotropic polypeptide (GIP) was the first incretin identified and plays an essential role in the maintenance of glucose tolerance in healthy humans. Until recently GIP had not been developed as a therapeutic and thus has been overshadowed by the other incretin, glucagon-like peptide 1 (GLP-1), which is the basis for several successful drugs to treat diabetes and obesity. However, there has been a rekindling of interest in GIP biology in recent years, in great part due to pharmacology demonstrating that both GIPR agonism and antagonism may be beneficial in treating obesity and diabetes. This apparent paradox has reinvigorated the field, led to new lines of investigation, and deeper understanding of GIP. Scope of Review: In this review, we provide a detailed overview on the multifaceted nature of GIP biology and discuss the therapeutic implications of GIPR signal modification on various diseases. Major Conclusions: Following its classification as an incretin hormone, GIP has emerged as a pleiotropic hormone with a variety of metabolic effects outside the endocrine pancreas. The numerous beneficial effects of GIPR signal modification render the peptide an interesting candidate for the development of pharmacotherapies to treat obesity, diabetes, drug-induced nausea and both bone and neurodegenerative disorders.</p>}},
author = {{Müller, Timo D. and Adriaenssens, Alice and Ahrén, Bo and Blüher, Matthias and Birkenfeld, Andreas L. and Campbell, Jonathan E. and Coghlan, Matthew P. and D'Alessio, David and Deacon, Carolyn F. and DelPrato, Stefano and Douros, Jonathan D. and Drucker, Daniel J. and Figueredo Burgos, Natalie S. and Flatt, Peter R. and Finan, Brian and Gimeno, Ruth E. and Gribble, Fiona M. and Hayes, Matthew R. and Hölscher, Christian and Holst, Jens J. and Knerr, Patrick J. and Knop, Filip K. and Kusminski, Christine M. and Liskiewicz, Arkadiusz and Mabilleau, Guillaume and Mowery, Stephanie A. and Nauck, Michael A. and Novikoff, Aaron and Reimann, Frank and Roberts, Anna G. and Rosenkilde, Mette M. and Samms, Ricardo J. and Scherer, Philip E. and Seeley, Randy J. and Sloop, Kyle W. and Wolfrum, Christian and Wootten, Denise and DiMarchi, Richard D. and Tschöp, Matthias H.}},
issn = {{2212-8778}},
keywords = {{Diabetes; GIP; GLP-1; Incretin; Insulin; Obesity}},
language = {{eng}},
publisher = {{Elsevier}},
series = {{Molecular Metabolism}},
title = {{Glucose-dependent insulinotropic polypeptide (GIP)}},
url = {{http://dx.doi.org/10.1016/j.molmet.2025.102118}},
doi = {{10.1016/j.molmet.2025.102118}},
volume = {{95}},
year = {{2025}},
}