{"@context":{"@vocab":"https://cir.nii.ac.jp/schema/1.0/","rdfs":"http://www.w3.org/2000/01/rdf-schema#","dc":"http://purl.org/dc/elements/1.1/","dcterms":"http://purl.org/dc/terms/","foaf":"http://xmlns.com/foaf/0.1/","prism":"http://prismstandard.org/namespaces/basic/2.0/","cinii":"http://ci.nii.ac.jp/ns/1.0/","datacite":"https://schema.datacite.org/meta/kernel-4/","ndl":"http://ndl.go.jp/dcndl/terms/","jpcoar":"https://github.com/JPCOAR/schema/blob/master/2.0/"},"@id":"https://cir.nii.ac.jp/crid/1362825895776671872.json","@type":"Article","productIdentifier":[{"identifier":{"@type":"DOI","@value":"10.1126/science.1128294"}},{"identifier":{"@type":"URI","@value":"https://www.science.org/doi/pdf/10.1126/science.1128294"}},{"identifier":{"@type":"NAID","@value":"80018956737"}}],"dc:title":[{"@value":"Chemical Chaperones Reduce ER Stress and Restore Glucose Homeostasis in a Mouse Model of Type 2 Diabetes"}],"description":[{"type":"abstract","notation":[{"@value":"<jats:p>Endoplasmic reticulum (ER) stress is a key link between obesity, insulin resistance, and type 2 diabetes. Here, we provide evidence that this mechanistic link can be exploited for therapeutic purposes with orally active chemical chaperones. 4-Phenyl butyric acid and taurine-conjugated ursodeoxycholic acid alleviated ER stress in cells and whole animals. Treatment of obese and diabetic mice with these compounds resulted in normalization of hyperglycemia, restoration of systemic insulin sensitivity, resolution of fatty liver disease, and enhancement of insulin action in liver, muscle, and adipose tissues. Our results demonstrate that chemical chaperones enhance the adaptive capacity of the ER and act as potent antidiabetic modalities with potential application in the treatment of type 2 diabetes.</jats:p>"}]}],"creator":[{"@id":"https://cir.nii.ac.jp/crid/1382825895776671747","@type":"Researcher","foaf:name":[{"@value":"Umut Özcan"}],"jpcoar:affiliationName":[{"@value":"Department of Genetics and Complex Diseases, Harvard School of Public Health, Harvard University, Boston, MA 02115, USA."}]},{"@id":"https://cir.nii.ac.jp/crid/1382825895776671744","@type":"Researcher","foaf:name":[{"@value":"Erkan Yilmaz"}],"jpcoar:affiliationName":[{"@value":"Department of Genetics and Complex Diseases, Harvard School of Public Health, Harvard University, Boston, MA 02115, USA."}]},{"@id":"https://cir.nii.ac.jp/crid/1382825895776671748","@type":"Researcher","foaf:name":[{"@value":"Lale Özcan"}],"jpcoar:affiliationName":[{"@value":"Department of Genetics and Complex Diseases, Harvard School of Public Health, Harvard University, Boston, MA 02115, USA."}]},{"@id":"https://cir.nii.ac.jp/crid/1382825895776671745","@type":"Researcher","foaf:name":[{"@value":"Masato Furuhashi"}],"jpcoar:affiliationName":[{"@value":"Department of Genetics and Complex Diseases, Harvard School of Public Health, Harvard University, Boston, MA 02115, USA."}]},{"@id":"https://cir.nii.ac.jp/crid/1382825895776671873","@type":"Researcher","foaf:name":[{"@value":"Eric Vaillancourt"}],"jpcoar:affiliationName":[{"@value":"Department of Genetics and Complex Diseases, Harvard School of Public Health, Harvard University, Boston, MA 02115, USA."}]},{"@id":"https://cir.nii.ac.jp/crid/1382825895776671749","@type":"Researcher","foaf:name":[{"@value":"Ross O. Smith"}],"jpcoar:affiliationName":[{"@value":"Department of Genetics and Complex Diseases, Harvard School of Public Health, Harvard University, Boston, MA 02115, USA."}]},{"@id":"https://cir.nii.ac.jp/crid/1382825895776671872","@type":"Researcher","foaf:name":[{"@value":"Cem Z. Görgün"}],"jpcoar:affiliationName":[{"@value":"Department of Genetics and Complex Diseases, Harvard School of Public Health, Harvard University, Boston, MA 02115, USA."}]},{"@id":"https://cir.nii.ac.jp/crid/1382825895776671746","@type":"Researcher","foaf:name":[{"@value":"Gökhan S. Hotamisligil"}],"jpcoar:affiliationName":[{"@value":"Department of Genetics and Complex Diseases, Harvard School of Public Health, Harvard University, Boston, MA 02115, USA."}]}],"publication":{"publicationIdentifier":[{"@type":"PISSN","@value":"00368075"},{"@type":"EISSN","@value":"10959203"}],"prism:publicationName":[{"@value":"Science"}],"dc:publisher":[{"@value":"American Association for the Advancement of Science (AAAS)"}],"prism:publicationDate":"2006-08-25","prism:volume":"313","prism:number":"5790","prism:startingPage":"1137","prism:endingPage":"1140"},"reviewed":"false","url":[{"@id":"https://www.science.org/doi/pdf/10.1126/science.1128294"}],"createdAt":"2006-08-24","modifiedAt":"2024-01-09","relatedProduct":[{"@id":"https://cir.nii.ac.jp/crid/1050002212669077376","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@language":"ja","@value":"Protective role of podocyte autophagy against glomerular endothelial 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