dc.creatorAtorrasagasti, María Catalina
dc.creatorOnorato, Agostina Mariana
dc.creatorGimeno, Maria Laura
dc.creatorAndreone, Luz
dc.creatorGarcía, Mariana Gabriela
dc.creatorMalvicini, Mariana
dc.creatorFiore, Esteban Juan
dc.creatorBayo Fina, Juan Miguel
dc.creatorPerone, Marcelo Javier
dc.creatorMazzolini Rizzo, Guillermo Daniel
dc.date.accessioned2021-02-03T11:39:43Z
dc.date.accessioned2022-10-15T00:50:54Z
dc.date.available2021-02-03T11:39:43Z
dc.date.available2022-10-15T00:50:54Z
dc.date.created2021-02-03T11:39:43Z
dc.date.issued2019-01
dc.identifierAtorrasagasti, María Catalina; Onorato, Agostina Mariana; Gimeno, Maria Laura; Andreone, Luz; García, Mariana Gabriela; et al.; SPARC is required for the maintenance of glucose homeostasis and insulin secretion in mice; Portland Press; Clinical Science; 133; 2; 1-2019; 351-365
dc.identifier0143-5221
dc.identifierhttp://hdl.handle.net/11336/124559
dc.identifierCONICET Digital
dc.identifierCONICET
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/4326777
dc.description.abstractObesity, metabolic syndrome, and type 2 diabetes, three strongly interrelated diseases, are associated to increased morbidity and mortality worldwide. The pathogenesis of obesity-associated disorders is still under study. Secreted protein acidic and rich in cysteine (SPARC) is a matricellular glycoprotein expressed in many cell types including adipocytes, parenchymal, and non-parenchymal hepatic cells and pancreatic cells. Studies have demonstrated that SPARC inhibits adipogenesis and promotes insulin resistance; in addition, circulating SPARC levels were positively correlated with body mass index in obese individuals. Therefore, SPARC is being proposed as a key factor in the pathogenesis of obesity-associated disorders. The aim of this study is to elucidate the role of SPARC in glucose homeostasis. We show here that SPARC null (SPARC −/− ) mice displayed an abnormal insulin-regulated glucose metabolism. SPARC −/− mice presented an increased adipose tissue deposition and an impaired glucose homeostasis as animals aged. In addition, the absence of SPARC worsens high-fat diet-induced diabetes in mice. Interestingly, although SPARC −/− mice on high-fat diet were sensitive to insulin they showed an impaired insulin secretion capacity. Of note, the expression of glucose transporter 2 in islets of SPARC −/− mice was dramatically reduced. The present study provides the first evidence that deleted SPARC expression causes diabetes in mice. Thus, SPARC deficient mice constitute a valuable model for studies concerning obesity and its related metabolic complications, including diabetes.
dc.languageeng
dc.publisherPortland Press
dc.relationinfo:eu-repo/semantics/altIdentifier/url/https://portlandpress.com/clinsci/article-abstract/133/2/351/111047/SPARC-is-required-for-the-maintenance-of-glucose?redirectedFrom=fulltext
dc.relationinfo:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1042/CS20180714
dc.rightshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectSPARC
dc.subjectGLUCOSE HOMEOSTASIS
dc.subjectINSULIN SECRETION
dc.titleSPARC is required for the maintenance of glucose homeostasis and insulin secretion in mice
dc.typeinfo:eu-repo/semantics/article
dc.typeinfo:ar-repo/semantics/artículo
dc.typeinfo:eu-repo/semantics/publishedVersion


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