Palmitate-Induced β-Cell Dysfunction Is Associated with Excessive NO Production and Is Reversed by Thiazolidinedione-Mediated Inhibition of GPR40 Transduction Mechanisms

BACKGROUND: Type 2 diabetes often displays hyperlipidemia. We examined palmitate effects on pancreatic islet function in relation to FFA receptor GPR40, NO generation, insulin release, and the PPARγ agonistic thiazolidinedione, rosiglitazone. PRINCIPAL FINDINGS: Rosiglitazone suppressed acute palmit...

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Detalhes bibliográficos
Main Authors: Meidute Abaraviciene, Sandra, Lundquist, Ingmar, Galvanovskis, Juris, Flodgren, Erik, Olde, Björn, Salehi, Albert
Formato: Artigo
Idioma:Inglês
Publicado em: Public Library of Science 2008
Assuntos:
Research Article
Acesso em linha:https://ncbi.nlm.nih.gov/pmc/articles/PMC2366067/
https://ncbi.nlm.nih.gov/pubmed/18478115
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1371/journal.pone.0002182
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