Cited by 191Diabetes Treatment and ManagementRegulation of Appetite and ObesityPancreatic function and diabetes

On the physiology of GIP and GLP-1

Holst, J. J.·2004·Hormone and Metabolic Research

Abstract

Recent studies have indicated that GIP and GLP-1 are about as important as each other in the incretin effect, being released rapidly after meals and being active already at fasting glucose levels. Although the density of GLP-1 producing cells is higher distally, GlP-1 is normally secreted by jejunal L-cells, explaining the rapid onset of secretion. Moreover, many endocrine cells in the small intestine appear to produce both GIP and GLP-1. Both are metabolized rapidly by the dipeptidyl peptidase IV enzyme, but unlike GIP, about 90 % of GLP-1 is degraded before it reaches the systemic circulation. Apparently, before it is degraded, GLP-1 activates sensory afferents in the gastrointestinal mucosa with cell bodies in the nodose ganglion, signaling onwards to the brain stem and the hypothalamus. A similar mechanism seems to be involved in GLP-1's effect on gastrointestinal motility and secretion, and perhaps its actions on appetite and food intake, all of which may be even more physiologically important than its effects on the beta cells. Cardiovascular and neuroprotective actions of GLP-1 have also recently been reported. Regarding GIP, several lines of evidence suggest that GIP, in addition to its incretin effects, may affect lipid metabolism and promote lipid storage.

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Crossref · 10.1055/s-2004-826158

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  • Luminal glucose exposure releases GIP from proximal K-cells and GLP-1 and GLP-2 from more distal L-cells.

    “These signals include release of the gut peptides glucosedependent insulinotropic polypeptide (GIP) from K-cells located in the proximal intestine and glucagon-like peptide-1 and 2 (GLP-1, GLP-2) from L-cells located in more distal regions of the intestine (5,6)”

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Authors
Holst, J. J.
Affiliations
University of Copenhagen (DK)
Corresponding author
Holst, J. J.
Venue
Hormone and Metabolic Research
Published
2004-11
Volume
36
Issue
11/12
Pages
747-754
ISSN
  • 0018-5043 (ISSN-L)
  • 1439-4286
OpenAlex
W2074835704
Cited by
189
References
0
Citations by year
2026: 1 · 2025: 7 · 2024: 7 · 2023: 2 · 2022: 2 · 2021: 5 · 2020: 7 · 2019: 8 · 2018: 7 · 2017: 6 · 2016: 5 · 2015: 11 · 2014: 16 · 2013: 14 · 2012: 11
FWCI
7.23
Type
journal article
Language
de
Open access
closed
Locations
  • Hormone and Metabolic Research (publishedVersion)
  • PubMed (publishedVersion)
  • Research at the University of Copenhagen (University of Copenhagen) (publishedVersion)
  • Research at the University of Copenhagen (University of Copenhagen) (submittedVersion)
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
Keywords
glucagon-like peptide-1, glucose-dependent insulinotropic polypeptide, incretin effect, dipeptidyl peptidase IV, GLP-1 receptor, nodose ganglion, gastrointestinal motility, beta-cell function, cardiovascular effects, neuroprotection, lipid metabolism, fat deposition
MeSH terms
Animals, Appetite, Cardiovascular System, Gastric Inhibitory Polypeptide, Gastrointestinal Motility, Glucagon, Humans, Intestine, Small, Jejunum, Neurosecretory Systems, Peptide Fragments, Protein Precursors, Mice, Knockout, Mice, Glucagon-Like Peptide 1

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