RGD Reference Report - Glucose intolerance caused by a defect in the entero-insular axis: a study in gastric inhibitory polypeptide receptor knockout mice. - Rat Genome Database

Send us a Message
Submit Data |  Help |  Video Tutorials |  News |  Publications |  Download |  REST API |  Citing RGD |  Contact   
Search RGD Grant Resources Citing RGD About Us Contact Us
Genes Variants Community Projects QTLs Strains Markers Genome Information Ontologies Cell Lines References Download Submit Data
OntoMate (Literature Search) JBrowse (Genome Browser) Synteny Browser (VCMap) Variant Visualizer Multi-Ontology Enrichment (MOET) Gene-Ortholog Location Finder (GOLF) InterViewer (Protein-Protein Interactions) PhenoMiner (Quatitative Phenotypes) Gene Annotator OLGA (Gene List Generator) AllianceMine GViewer (Genome Viewer)
Aging & Age-Related Disease Cancer & Neoplastic Disease Cardiovascular Disease Coronavirus Disease Developmental Disease Diabetes Hematologic Disease Immune & Inflammatory Disease Infectious Disease Liver Disease Neurological Disease Obesity & Metabolic Syndrome Renal Disease Respiratory Disease Sensory Organ Disease
Find Models Genetic Models Autism Models Rat PhenoMiner (Quantitative Phenotypes) Chinchilla PhenoMiner Expected Ranges (Quantitative Phenotype) PhenoMiner Term Comparison Hybrid Rat Diversity Panel Phenotypes Phenotypes in Other Animal Models Animal Husbandry Strain Medical Records Phylogenetics Strain Availability Calendar Rats 101 Submissions Photo Archive
Pathways
Rat Community Forum Directory of Rat Laboratories Video Tutorials News RGD Publications RGD Presentations Archive Nomenclature Guidelines Resource Links Laboratory Resources Employment Resources
Advanced Search (OLGA)

Glucose intolerance caused by a defect in the entero-insular axis: a study in gastric inhibitory polypeptide receptor knockout mice.

Authors: Miyawaki, K  Yamada, Y  Yano, H  Niwa, H  Ban, N  Ihara, Y  Kubota, A  Fujimoto, S  Kajikawa, M  Kuroe, A  Tsuda, K  Hashimoto, H  Yamashita, T  Jomori, T  Tashiro, F  Miyazaki, J  Seino, Y 
Citation: Miyawaki K, etal., Proc Natl Acad Sci U S A 1999 Dec 21;96(26):14843-7.
RGD ID: 737713
Pubmed: PMID:10611300   (View Abstract at PubMed)
PMCID: PMC24735   (View Article at PubMed Central)

Mice with a targeted mutation of the gastric inhibitory polypeptide (GIP) receptor gene (GIPR) were generated to determine the role of GIP as a mediator of signals from the gut to pancreatic beta cells. GIPR-/- mice have higher blood glucose levels with impaired initial insulin response after oral glucose load. Although blood glucose levels after meal ingestion are not increased by high-fat diet in GIPR+/+ mice because of compensatory higher insulin secretion, they are significantly increased in GIPR-/- mice because of the lack of such enhancement. Accordingly, early insulin secretion mediated by GIP determines glucose tolerance after oral glucose load in vivo, and because GIP plays an important role in the compensatory enhancement of insulin secretion produced by a high insulin demand, a defect in this entero-insular axis may contribute to the pathogenesis of diabetes.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
GIPRHumanglucose intolerance  ISOGipr (Mus musculus) RGD 
GiprRatglucose intolerance  ISOGipr (Mus musculus) RGD 
GiprMouseglucose intolerance  IMP  RGD 
GIPRHumanhyperglycemia  ISOGipr (Mus musculus) RGD 
GiprRathyperglycemia  ISOGipr (Mus musculus) RGD 
GiprMousehyperglycemia  IMP  RGD 

Objects Annotated

Genes (Rattus norvegicus)
Gipr  (gastric inhibitory polypeptide receptor)

Genes (Mus musculus)
Gipr  (gastric inhibitory polypeptide receptor)

Genes (Homo sapiens)
GIPR  (gastric inhibitory polypeptide receptor)

Objects referenced in this article
Gene Edn1 endothelin 1 Mus musculus

Additional Information