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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Hansen, L. S. Holst, J. J. Christensen, M. Sparre-ulrich, A. H. Svendsen, B. Hartmann, B. Knop, F. K. Rosenkilde, M. M. |
| Description | Author Affiliation: Sparre-Ulrich AH ( Department of Neuroscience and Pharmacology, Faculty of Health and Medical Sciences, The Panum Institute, University of Copenhagen, Copenhagen, Denmark.); Hansen LS ( NNF Center for Basic Metabolic Research, Copenhagen, Denmark.); Svendsen B ( Department of Neuroscience and Pharmacology, Faculty of Health and Medical Sciences, The Panum Institute, University of Copenhagen, Copenhagen, Denmark.); Christensen M ( NNF Center for Basic Metabolic Research, Copenhagen, Denmark.); Knop FK ( Center for Diabetes Research, Gentofte Hospital, University of Copenhagen, Copenhagen, Denmark.); Hartmann B ( NNF Center for Basic Metabolic Research, Copenhagen, Denmark.); Holst JJ ( Center for Diabetes Research, Gentofte Hospital, University of Copenhagen, Copenhagen, Denmark.); Rosenkilde MM ( Center for Diabetes Research, Gentofte Hospital, University of Copenhagen, Copenhagen, Denmark.) |
| Abstract | Background and Purpose Specific, high potency receptor antagonists are valuable tools when evaluating animal and human physiology. Within the glucose‐dependent, insulinotropic polypeptide (GIP) system, considerable attention has been given to the presumed GIP receptor antagonist, (Pro3)GIP, and its effect in murine studies. We conducted a pharmacological analysis of this ligand including interspecies differences between the rodent and human GIP system. Experimental Approach Transiently transfected COS‐7 cells were assessed for cAMP accumulation upon ligand stimulation and assayed in competition binding using $^{125}I‐human$ GIP. Using isolated perfused pancreata both from wild type and GIP receptor‐deficient rodents, insulin‐releasing, glucagon‐releasing and somatostatin‐releasing properties in response to species‐specific GIP and (Pro3)GIP analogues were evaluated. Key Results Human (Pro3)GIP is a full agonist at human GIP receptors with similar efficacy (E $_{max})$ for cAMP production as human GIP, while both rat and mouse(Pro3)GIP were partial agonists on their corresponding receptors. Rodent GIPs are more potent and efficacious at their receptors than human GIP. In perfused pancreata in the presence of 7 mM glucose, both rodent (Pro3)GIP analogues induced modest insulin, glucagon and somatostatin secretion, corresponding to the partial agonist activities observed in cAMP production. Conclusions and Implications When evaluating new compounds, it is important to consider interspecies differences both at the receptor and ligand level. Thus, in rodent models, human GIP is a comparatively weak partial agonist. Human (Pro3)GIP was not an antagonist at human GIP receptors, so there is still a need for a potent antagonist in order to elucidate the physiology of human GIP. |
| ISSN | 00071188 |
| e-ISSN | 14765381 |
| Journal | British Journal of Pharmacology |
| Issue Number | 1 |
| Volume Number | 173 |
| Language | English |
| Publisher | Wiley Online Library(on behalf of The British Pharmacological Society) |
| Publisher Date | 2016-01-01 |
| Publisher Place | Great Britain (UK) |
| Access Restriction | Open |
| Subject Keyword | Drug Partial Agonism Gastric Inhibitory Polypeptide Pharmacology Receptors, Gastrointestinal Hormone Agonists Antagonists & Inhibitors Animals Binding, Competitive Drug Effects COS Cells Cercopithecus Aethiops Cyclic AMP Metabolism Dose-Response Relationship, Drug Analogs & Derivatives Glucagon Insulin Iodine Radioisotopes Mice Pancreas Radioligand Assay Somatostatin Species Specificity Comparative Study Research Support, Non-U.S. Gov't |
| Content Type | Text |
| Resource Type | Article |
| Subject | Pharmacology |
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