RDF/XMLNTriplesTurtleShow queryShare
SubjectPredicateObject
http://purl.uniprot.org/citations/22275755http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/22275755http://www.w3.org/2000/01/rdf-schema#comment"TRPM2 Ca(2+)-permeable cation channel is widely expressed and activated by markers of cellular stress. Since inflammation and stress play a major role in insulin resistance, we examined the role of TRPM2 Ca(2+) channel in glucose metabolism. A 2-h hyperinsulinemic euglycemic clamp was performed in TRPM2-deficient (KO) and wild-type mice to assess insulin sensitivity. To examine the effects of diet-induced obesity, mice were fed a high-fat diet for 4-10 mo, and metabolic cage and clamp studies were conducted in conscious mice. TRPM2-KO mice were more insulin sensitive partly because of increased glucose metabolism in peripheral organs. After 4 mo of high-fat feeding, TRPM2-KO mice were resistant to diet-induced obesity, and this was associated with increased energy expenditure and elevated expressions of PGC-1α, PGC-1β, PPARα, ERRα, TFAM, and MCAD in white adipose tissue. Hyperinsulinemic euglycemic clamps showed that TRPM2-KO mice were more insulin sensitive, with increased Akt and GSK-3β phosphorylation in heart. Obesity-mediated inflammation in adipose tissue and liver was attenuated in TRPM2-KO mice. Overall, TRPM2 deletion protected mice from developing diet-induced obesity and insulin resistance. Our findings identify a novel role of TRPM2 Ca(2+) channel in the regulation of energy expenditure, inflammation, and insulin resistance."xsd:string
http://purl.uniprot.org/citations/22275755http://purl.org/dc/terms/identifier"doi:10.1152/ajpendo.00239.2011"xsd:string
http://purl.uniprot.org/citations/22275755http://purl.uniprot.org/core/author"Ma Z."xsd:string
http://purl.uniprot.org/citations/22275755http://purl.uniprot.org/core/author"Lee Y."xsd:string
http://purl.uniprot.org/citations/22275755http://purl.uniprot.org/core/author"Lee E."xsd:string
http://purl.uniprot.org/citations/22275755http://purl.uniprot.org/core/author"Zhang W."xsd:string
http://purl.uniprot.org/citations/22275755http://purl.uniprot.org/core/author"Zhang Z."xsd:string
http://purl.uniprot.org/citations/22275755http://purl.uniprot.org/core/author"Kim J.K."xsd:string
http://purl.uniprot.org/citations/22275755http://purl.uniprot.org/core/author"Ko H.J."xsd:string
http://purl.uniprot.org/citations/22275755http://purl.uniprot.org/core/author"Friedline R.H."xsd:string
http://purl.uniprot.org/citations/22275755http://purl.uniprot.org/core/author"Jun J."xsd:string
http://purl.uniprot.org/citations/22275755http://purl.uniprot.org/core/author"Morrison A."xsd:string
http://purl.uniprot.org/citations/22275755http://purl.uniprot.org/core/author"Jung D.Y."xsd:string
http://purl.uniprot.org/citations/22275755http://purl.uniprot.org/core/author"Chapman K."xsd:string
http://purl.uniprot.org/citations/22275755http://purl.uniprot.org/core/author"Cooper M.P."xsd:string
http://purl.uniprot.org/citations/22275755http://purl.uniprot.org/core/author"Kim F."xsd:string
http://purl.uniprot.org/citations/22275755http://purl.uniprot.org/core/author"Miller B.A."xsd:string
http://purl.uniprot.org/citations/22275755http://purl.uniprot.org/core/author"Tsitsilianos N."xsd:string
http://purl.uniprot.org/citations/22275755http://purl.uniprot.org/core/date"2012"xsd:gYear
http://purl.uniprot.org/citations/22275755http://purl.uniprot.org/core/name"Am J Physiol Endocrinol Metab"xsd:string
http://purl.uniprot.org/citations/22275755http://purl.uniprot.org/core/pages"E807-16"xsd:string
http://purl.uniprot.org/citations/22275755http://purl.uniprot.org/core/title"TRPM2 Ca2+ channel regulates energy balance and glucose metabolism."xsd:string
http://purl.uniprot.org/citations/22275755http://purl.uniprot.org/core/volume"302"xsd:string
http://purl.uniprot.org/citations/22275755http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/22275755