RDF/XMLNTriplesTurtleShow queryShare
SubjectPredicateObject
http://purl.uniprot.org/citations/20685876http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/20685876http://www.w3.org/2000/01/rdf-schema#comment"Glucagon-like peptide-1 augments nutrient-stimulated insulin secretion. Chow-fed mice lacking the glucagon-like peptide-1 receptor (Glp1r) exhibit enhanced insulin-stimulated muscle glucose uptake but impaired suppression of endogenous glucose appearance (endoRa). This proposes a novel role for the Glp1r to regulate the balance of glucose disposal in muscle and liver by modulating insulin action. Whether this is maintained in an insulin-resistant state is unknown. The present studies tested the hypothesis that disruption of Glp1r expression overcomes high-fat (HF) diet-induced muscle insulin resistance and exacerbates HF diet-induced hepatic insulin resistance. Mice with a functional disruption of the Glp1r (Glp1r-/-) were compared with wild-type littermates (Glp1r+/+) after 12 wk on a regular chow diet or a HF diet. Arterial and venous catheters were implanted for sampling and infusions. Hyperinsulinemic-euglycemic clamps were performed on weight-matched male mice. [3-(3)H]glucose was used to determine glucose turnover, and 2[14C]deoxyglucose was used to measure the glucose metabolic index, an indicator of glucose uptake. Glp1r-/-mice exhibited increased glucose disappearance and muscle glucose metabolic index on either diet. This was associated with enhanced activation of muscle Akt and AMP-activated protein kinase and reduced muscle triglycerides in HF-fed Glp1r-/- mice. Chow-fed Glp1r-/-mice exhibited impaired suppression of endoRa and hepatic insulin signaling. In contrast, HF-fed Glp1r-/-mice exhibited improved suppression of endoRa and hepatic Akt activation. This was associated with decreased hepatic triglycerides and impaired activation of sterol regulatory element-binding protein-1. These results show that mice lacking the Glp1r are protected from HF diet-induced muscle and hepatic insulin resistance independent of effects on total fat mass."xsd:string
http://purl.uniprot.org/citations/20685876http://purl.org/dc/terms/identifier"doi:10.1210/en.2010-0289"xsd:string
http://purl.uniprot.org/citations/20685876http://purl.uniprot.org/core/author"Wasserman D.H."xsd:string
http://purl.uniprot.org/citations/20685876http://purl.uniprot.org/core/author"Drucker D.J."xsd:string
http://purl.uniprot.org/citations/20685876http://purl.uniprot.org/core/author"Ayala J.E."xsd:string
http://purl.uniprot.org/citations/20685876http://purl.uniprot.org/core/author"Bracy D.P."xsd:string
http://purl.uniprot.org/citations/20685876http://purl.uniprot.org/core/author"James F.D."xsd:string
http://purl.uniprot.org/citations/20685876http://purl.uniprot.org/core/author"Burmeister M.A."xsd:string
http://purl.uniprot.org/citations/20685876http://purl.uniprot.org/core/date"2010"xsd:gYear
http://purl.uniprot.org/citations/20685876http://purl.uniprot.org/core/name"Endocrinology"xsd:string
http://purl.uniprot.org/citations/20685876http://purl.uniprot.org/core/pages"4678-4687"xsd:string
http://purl.uniprot.org/citations/20685876http://purl.uniprot.org/core/title"Glucagon-like peptide-1 receptor knockout mice are protected from high-fat diet-induced insulin resistance."xsd:string
http://purl.uniprot.org/citations/20685876http://purl.uniprot.org/core/volume"151"xsd:string
http://purl.uniprot.org/citations/20685876http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/20685876
http://purl.uniprot.org/citations/20685876http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/20685876
http://purl.uniprot.org/uniprot/#_B7ZP48-mappedCitation-20685876http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/20685876
http://purl.uniprot.org/uniprot/#_Q104P0-mappedCitation-20685876http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/20685876
http://purl.uniprot.org/uniprot/#_Q3ZAW0-mappedCitation-20685876http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/20685876
http://purl.uniprot.org/uniprot/#_O35659-mappedCitation-20685876http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/20685876
http://purl.uniprot.org/uniprot/O35659http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/20685876
http://purl.uniprot.org/uniprot/Q104P0http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/20685876
http://purl.uniprot.org/uniprot/Q3ZAW0http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/20685876
http://purl.uniprot.org/uniprot/B7ZP48http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/20685876