Preservation of incretin activity after removal of gastric inhibitory polypeptide (GIP) from rat gut extracts by immunoadsorption
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The action of watery rat gut extracts on glucose-induced insulin release in anaesthetized rats was examined before and after removal of GIP by immunoadsorption. Infusions of GIP-containing rat gut extracts nearly doubled the insulin release induced by intravenous glucose (1 g X kg -1 X h -1). Peak insulin secretion was 98 +/- 11 mU/l (mean +/- SEM) after intravenous glucose and increased to 178 +/- 16 mU/l following infusion of glucose plus gut extract (p less than 0.005). After injection of GIP antiserum in sufficient amounts to neutralize the GIP activity in the gut extract preparation, the additional insulin release due to the gut extract was reduced by only 30%. After complete removal of GIP from gut extracts by immuno-absorption, more than 50% of the incretin effect remained. These data suggest that the insulinotropic activity of rat gut extracts can only be partially related to GIP. The existence of additional insulinotropic gut factors which may also be released following oral glucose is postulated.
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Central GIPR agonism reduces the emetic effect of GLP-1R agonism and promotes weight loss by suppressing food intake.
“and that central GIPR agonism ameliorates the emetic effect of GLP-1 receptor (GLP-1R) agonism44, and stimulates weight loss through inhibition of food intake45,46.”
From Transforming obesity: The advancement of multi-receptor drugs (2024) · cites this paper as [44]
The Abstract and Discussion describe insulin release in rats after GIP was removed from gut extracts; no page numbers are available in our copy. Searches for central GIPR agonism, emesis, food intake, and weight loss found no passage addressing either effect attributed to the source. (LLM, conf=0.76)
Experimental — accuracy not yet measuredIn musk shrews and mice, giving a GIPR mono-agonist reduced the nausea and vomiting caused by GLP-1R agonism.
“studies in musk shrews and mice revealed that GIPR mono-agonist administration attenuated the emetic effect of GLP-1R agonism44,131”
From Transforming obesity: The advancement of multi-receptor drugs (2024) · cites this paper as [44]
The Abstract and Discussion describe GIP removal from rat gut extracts and its effect on glucose-induced insulin release; neither addresses emesis. Searches for musk shrews, mice, nausea or vomiting, and GIPR and GLP-1R agonism found no passage supporting the attributed finding. Page numbers were not available in our copy. (LLM, conf=0.78)
Experimental — accuracy not yet measured
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- Authors
- Ebert, R., Unger, H., & Creutzfeldt, W.
- Affiliations
- University of Göttingen (DE)
- Universitätsmedizin Göttingen (DE)
- Venue
- Diabetologia
- Published
- 1983-06
- Volume
- 24
- Issue
- 6
- Pages
- 449-54
- ISSN
- 0012-186X (ISSN-L)
- 1432-0428
- OpenAlex
- W2076998384
- Cited by
- 120
- References
- 37
- Citations by year
- 2026: 9 · 2025: 3 · 2024: 6 · 2023: 1 · 2022: 4 · 2021: 4 · 2020: 4 · 2019: 5 · 2017: 2 · 2016: 2 · 2015: 1 · 2014: 1 · 2013: 3 · 2012: 2
- FWCI
- 4.28
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Diabetologia (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Deutsche Forschungsgemeinschaft
- Topics
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
- Keywords
- glucose-dependent insulinotropic polypeptide, insulin secretion, immunoadsorption, glucose-induced insulin release, oral glucose, rats
- MeSH terms
- Insulin Secretion, Animals, Antibodies, Glucagon-Like Peptides, Gastric Inhibitory Polypeptide, Gastrointestinal Hormones, Glucagon, Glucose, Immunosorbent Techniques, Infusions, Parenteral, Insulin, Intestinal Mucosa, Male, Peptide Fragments, Peptides, Rats, Inbred Strains, Time Factors, Tissue Extracts, Rats, Glucagon-Like Peptide 1
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