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On the Physiology of GIP and GLP-1
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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“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)”
From Gut mechanisms linking intestinal sweet sensing to glycemic control (2018) · cites this paper as [6]
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Metadata
- Authors
- Holst, J. J.
- Affiliations
- University of Copenhagen (DK)
- Corresponding author
- Holst, J. J.
- ORCID
- Holst, J. J.
- Venue
- Hormone and Metabolic Research
- Publisher
- Georg Thieme Verlag KG
- 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 › Endocrinology, Diabetes and Metabolism › 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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