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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...
| Autores principales: | , , , , , |
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| Formato: | Texto |
| Lenguaje: | English |
| Publicado: |
Public Library of Science
2008
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| Materias: | |
| Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2366067/ https://www.ncbi.nlm.nih.gov/pubmed/18478115 http://dx.doi.org/10.1371/journal.pone.0002182 |