Palmitate-induced beta-cell dysfunction is associated with excessive NO production and is reversed by thiazolidinedione-mediated inhibition of GPR40 transduction mechanisms.

Palmitate-induced beta-cell dysfunction is associated with excessive NO production and is reversed by thiazolidinedione-mediated inhibition of GPR40 transduction mechanisms.

<h4>Background</h4>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 PPARgamma agonistic thiazolidinedione, rosiglitazone.<h4>Principal findings</h4...

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Autores principales: Sandra Meidute Abaraviciene, Ingmar Lundquist, Juris Galvanovskis, Erik Flodgren, Björn Olde, Albert Salehi
Formato: article
Lenguaje:EN
Publicado: Public Library of Science (PLoS) 2008
Materias:
Medicine
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Science
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Acceso en línea:https://doaj.org/article/4aa6fdb3020c4c02b4edec44f860efe3
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