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dc.contributor.author
Ferreira, María del Rosario
dc.contributor.author
Lombardo, Yolanda
dc.contributor.author
Chicco, Adriana Graciela
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dc.date.available
2020-04-01T17:40:55Z
dc.date.issued
2010-11
dc.identifier.citation
Ferreira, María del Rosario; Lombardo, Yolanda; Chicco, Adriana Graciela; Beta cell adaptation/dysfunction in an animal model of dyslipidemia and insulin resistance induced by the chronic administration of a sucrose-rich diet; Landes Bioscience Journal; Islets; 2; 6; 11-2010; 367-373
dc.identifier.issn
1938-2014
dc.identifier.uri
http://hdl.handle.net/11336/101540
dc.description.abstract
Glucose stimulated insulin secretion (GSIS) was different in rats chronically fed a sucrose-rich diet (SRD) for 3 or 30 wk. This work proposes possible mechanisms underlying insulin secretion changes from â-cell throughout these feeding periods. In isolated islets of rats fed the SRD or a control diet (CD) we examined: 1- the glucokinase and hexokinase activities and their protein mass expression; 2- pyruvate dehydrogenase activity; 3- uncoupling protein 2 (UCP2) and peroxisome proliferators-activated receptor ã (PPAR ã) protein mass expression. At 3 wk on diet the SRD-fed rats showed: a marked increase in the first peak of GSIS; increased glucokinase protein mass expression without changes in glucokinase and hexokinase activities; increased PPARã protein mass expression without changes in the UCP2 protein mass expression. No changes in either glucose oxidation and triglyceride content within the â-cell were observed. After 30 wk of feeding, a significant decrease of both glucokinase activity and its protein mass expression was accompanied by altered glucose oxidation, a triglyceride increase within the â-cell and a significant increase of PPARã and UCP2 protein mass expression. Moreover GSIS depicted an absence of the first peak with an increase in the second phase. Finally, the SRD chronic administration altered GSIS by different mechanisms depending on the time on diet. At an early stage, the increased protein mass expression of the glucokinase and a fatty acid cooperative effect inducing PPARã expression seem to be the mechanisms involved. At a late stage, glucolipotoxicity appears to be the cellular mechanism contributing to progressive â-cell dysfunction.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
Landes Bioscience Journal
dc.rights
info:eu-repo/semantics/openAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
Glucolipotoxicity
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Beta cell
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Dyslipidemia
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Sucrose-rich diet
dc.subject.classification
Fisiología
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dc.subject.classification
Medicina Básica
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CIENCIAS MÉDICAS Y DE LA SALUD
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dc.title
Beta cell adaptation/dysfunction in an animal model of dyslipidemia and insulin resistance induced by the chronic administration of a sucrose-rich diet
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
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info:eu-repo/semantics/publishedVersion
dc.date.updated
2020-03-27T13:44:41Z
dc.journal.volume
2
dc.journal.number
6
dc.journal.pagination
367-373
dc.journal.pais
Suecia
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dc.journal.ciudad
Estocolmo
dc.description.fil
Fil: Ferreira, María del Rosario. Universidad Nacional del Litoral. Facultad de Bioquímica y Ciencias Biológicas; Argentina
dc.description.fil
Fil: Lombardo, Yolanda. Universidad Nacional del Litoral. Facultad de Bioquímica y Ciencias Biológicas; Argentina
dc.description.fil
Fil: Chicco, Adriana Graciela. Universidad Nacional del Litoral. Facultad de Bioquímica y Ciencias Biológicas; Argentina
dc.journal.title
Islets
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.4161/isl.2.6.13869
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