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http://purl.uniprot.org/citations/21270251http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/21270251http://www.w3.org/2000/01/rdf-schema#comment"

Objective

To determine the role of glucagon action in the metabolic phenotype of untreated insulin deficiency.

Research design and methods

We compared pertinent clinical and metabolic parameters in glucagon receptor-null (Gcgr(-/-)) mice and wild-type (Gcgr(+/+)) controls after equivalent destruction of β-cells. We used a double dose of streptozotocin to maximize β-cell destruction.

Results

Gcgr(+/+) mice became hyperglycemic (>500 mg/dL), hyperketonemic, polyuric, and cachectic and had to be killed after 6 weeks. Despite comparable β-cell destruction in Gcgr(-/-) mice, none of the foregoing clinical or laboratory manifestations of diabetes appeared. There was marked α-cell hyperplasia and hyperglucagonemia (~1,200 pg/mL), but hepatic phosphorylated cAMP response element binding protein and phosphoenolpyruvate carboxykinase mRNA were profoundly reduced compared with Gcgr(+/+) mice with diabetes--evidence that glucagon action had been effectively blocked. Fasting glucose levels and oral and intraperitoneal glucose tolerance tests were normal. Both fasting and nonfasting free fatty acid levels and nonfasting β-hydroxy butyrate levels were lower.

Conclusions

We conclude that blocking glucagon action prevents the deadly metabolic and clinical derangements of type 1 diabetic mice."xsd:string
http://purl.uniprot.org/citations/21270251http://purl.org/dc/terms/identifier"doi:10.2337/db10-0426"xsd:string
http://purl.uniprot.org/citations/21270251http://purl.uniprot.org/core/author"Lee Y."xsd:string
http://purl.uniprot.org/citations/21270251http://purl.uniprot.org/core/author"Wang M.Y."xsd:string
http://purl.uniprot.org/citations/21270251http://purl.uniprot.org/core/author"Charron M.J."xsd:string
http://purl.uniprot.org/citations/21270251http://purl.uniprot.org/core/author"Du X.Q."xsd:string
http://purl.uniprot.org/citations/21270251http://purl.uniprot.org/core/author"Unger R.H."xsd:string
http://purl.uniprot.org/citations/21270251http://purl.uniprot.org/core/date"2011"xsd:gYear
http://purl.uniprot.org/citations/21270251http://purl.uniprot.org/core/name"Diabetes"xsd:string
http://purl.uniprot.org/citations/21270251http://purl.uniprot.org/core/pages"391-397"xsd:string
http://purl.uniprot.org/citations/21270251http://purl.uniprot.org/core/title"Glucagon receptor knockout prevents insulin-deficient type 1 diabetes in mice."xsd:string
http://purl.uniprot.org/citations/21270251http://purl.uniprot.org/core/volume"60"xsd:string
http://purl.uniprot.org/citations/21270251http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/21270251
http://purl.uniprot.org/citations/21270251http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/21270251
http://purl.uniprot.org/uniprot/#_Q3UN81-mappedCitation-21270251http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/21270251
http://purl.uniprot.org/uniprot/#_Q61606-mappedCitation-21270251http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/21270251
http://purl.uniprot.org/uniprot/#_Q548V8-mappedCitation-21270251http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/21270251
http://purl.uniprot.org/uniprot/Q3UN81http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/21270251
http://purl.uniprot.org/uniprot/Q548V8http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/21270251
http://purl.uniprot.org/uniprot/Q61606http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/21270251