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http://purl.uniprot.org/citations/23825225http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/23825225http://www.w3.org/2000/01/rdf-schema#comment"Previously, exchange protein directly activated by cAMP 2 (Epac2) and PKA were known to play a role in glucose-stimulated insulin secretion (GSIS) by pancreatic β cells. The present study shows that Epac1 mRNA is also expressed by β cells. Therefore, we generated mice and embryonic stem (ES) cells with deletion of the Epac1 gene to define its role in β-cell biology and metabolism. The homozygous Epac1-knockout (Epac1(-/-)) mice developed impaired glucose tolerance and GSIS with deranged islet cytoarchitecture, which was confirmed by isolated islets from adult Epac1(-/-) mice. Moreover, Epac1(-/-) mice developed more severe hyperglycemia with increased β-cell apoptosis and insulitis after multiple low-dose streptozotocin (MLDS; 40 mg/kg) treatment than Epac1(+/+) mice. Interestingly, Epac1(-/-) mice also showed metabolic defects, including increased respiratory exchange ratio (RER) and plasma triglyceride (TG), and more severe diet-induced obesity with insulin resistance, which may contributed to β-cell dysfunction. However, islets differentiated from Epac1(-/-) ES cells showed insulin secretion defect, reduced Glut2 and PDX-1 expression, and abolished GLP-1-stimulated PCNA induction, suggesting a role of Epac1 in β-cell function. The current study provides in vitro and in vivo evidence that Epac1 has an important role in GSIS of β cells and phenotype resembling metabolic syndrome."xsd:string
http://purl.uniprot.org/citations/23825225http://purl.org/dc/terms/identifier"doi:10.1096/fj.13-230433"xsd:string
http://purl.uniprot.org/citations/23825225http://purl.uniprot.org/core/author"Chen Y."xsd:string
http://purl.uniprot.org/citations/23825225http://purl.uniprot.org/core/author"Chung S.S."xsd:string
http://purl.uniprot.org/citations/23825225http://purl.uniprot.org/core/author"Bos J.L."xsd:string
http://purl.uniprot.org/citations/23825225http://purl.uniprot.org/core/author"Zhang X."xsd:string
http://purl.uniprot.org/citations/23825225http://purl.uniprot.org/core/author"Wang J."xsd:string
http://purl.uniprot.org/citations/23825225http://purl.uniprot.org/core/author"Xu A."xsd:string
http://purl.uniprot.org/citations/23825225http://purl.uniprot.org/core/author"Tam S."xsd:string
http://purl.uniprot.org/citations/23825225http://purl.uniprot.org/core/author"Lam K.S."xsd:string
http://purl.uniprot.org/citations/23825225http://purl.uniprot.org/core/author"Chung S.K."xsd:string
http://purl.uniprot.org/citations/23825225http://purl.uniprot.org/core/author"Lam A.K."xsd:string
http://purl.uniprot.org/citations/23825225http://purl.uniprot.org/core/author"Yeung P.K."xsd:string
http://purl.uniprot.org/citations/23825225http://purl.uniprot.org/core/author"Vanhoutte P.M."xsd:string
http://purl.uniprot.org/citations/23825225http://purl.uniprot.org/core/author"Lai A.K."xsd:string
http://purl.uniprot.org/citations/23825225http://purl.uniprot.org/core/author"Kai A.K."xsd:string
http://purl.uniprot.org/citations/23825225http://purl.uniprot.org/core/author"Tai A.C."xsd:string
http://purl.uniprot.org/citations/23825225http://purl.uniprot.org/core/date"2013"xsd:gYear
http://purl.uniprot.org/citations/23825225http://purl.uniprot.org/core/name"FASEB J"xsd:string
http://purl.uniprot.org/citations/23825225http://purl.uniprot.org/core/pages"4122-4135"xsd:string
http://purl.uniprot.org/citations/23825225http://purl.uniprot.org/core/title"Exchange protein activated by cAMP 1 (Epac1)-deficient mice develop beta-cell dysfunction and metabolic syndrome."xsd:string
http://purl.uniprot.org/citations/23825225http://purl.uniprot.org/core/volume"27"xsd:string
http://purl.uniprot.org/citations/23825225http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/23825225
http://purl.uniprot.org/citations/23825225http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/23825225