Fulltext

Fatty acids do not activate UCP2 in pancreatic beta cells: comparison with UCP1

Galetti, Sandrine ; Sarre, Alexandre ; Perreten, Hélène ; Produit-Zengaffinen, Nathalie ; Muzzin, Patrick ; Assimacopoulos-Jeannet, Françoise

In: Pflügers Archiv - European Journal of Physiology, 2009, vol. 457, no. 4, p. 931-940

Ajouter à la liste personnelle
    Titre
    • Fatty acids do not activate UCP2 in pancreatic beta cells: comparison with UCP1
    Auteur
    • Galetti, Sandrine. Department of Cell Physiology and Metabolism, Medical Faculty, University of Geneva, 1 rue Michel Servet, 1211, Geneva 4, Switzerland
    • Sarre, Alexandre. Department of Cell Physiology and Metabolism, Medical Faculty, University of Geneva, 1 rue Michel Servet, 1211, Geneva 4, Switzerland
    • Perreten, Hélène. Department of Cell Physiology and Metabolism, Medical Faculty, University of Geneva, 1 rue Michel Servet, 1211, Geneva 4, Switzerland
    • Produit-Zengaffinen, Nathalie. Department of Cell Physiology and Metabolism, Medical Faculty, University of Geneva, 1 rue Michel Servet, 1211, Geneva 4, Switzerland
    • Muzzin, Patrick. Department of Cell Physiology and Metabolism, Medical Faculty, University of Geneva, 1 rue Michel Servet, 1211, Geneva 4, Switzerland
    • Assimacopoulos-Jeannet, Françoise. Department of Cell Physiology and Metabolism, Medical Faculty, University of Geneva, 1 rue Michel Servet, 1211, Geneva 4, Switzerland
    Type de document
    • Postprint
    Langue
    • Anglais
    Publié dans
    • Pflügers Archiv - European Journal of Physiology, 2009, vol. 457, no. 4, p. 931-940. Springer-Verlag
    Autre version électronique
    Identifiant OAI-PMH
    • oai:doc.rero.ch:320071
    Summary
    UCP2 is expressed in pancreatic β cells where its postulated uncoupling activity will modulate glucose-induced changes in ATP/ADP ratio and insulin secretion. The consequences of UCP2 over/underexpression on β-cell function has mainly been studied in the basal state; however, a UCP has no uncoupling activity unless stimulated by fatty acids and/or reactive oxygen species. Here, UCP2 was overexpressed in INS-1 cells and parameters reflecting mitochondrial coupling measured in the basal state and after stimulation by fatty acids. For comparison, UCP1 was expressed to similar levels and the same parameters measured. Neither UCP1 expression nor UCP2 overexpression modified basal or glucose-stimulated metabolic changes. Upon addition of fatty acids, UCP1-expressing cells displayed the expected mitochondrial uncoupling effect, while UCP2 did not elicit any measurable change in mitochondrial function. Taken together, our data demonstrate that, in pancreatic β-cells, UCP2 has no uncoupling activity in the basal state or after fatty acid stimulation