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Mitochondrial fragmentation impairs insulin-dependent glucose uptake by modulating Akt activity through mitochondrial Ca2+ uptake

Authordc.contributor.authorDel Campo Sfeir, Andrea Estefanía 
Authordc.contributor.authorParra Ortíz, María Valentina es_CL
Authordc.contributor.authorVásquez Trincado, César Alonso es_CL
Authordc.contributor.authorGutiérrez, Tomás es_CL
Authordc.contributor.authorMorales, Pablo E. es_CL
Authordc.contributor.authorLópez Crisosto, Camila es_CL
Authordc.contributor.authorBravo Sagua, Roberto es_CL
Authordc.contributor.authorNavarro Márquez, Mario F. es_CL
Authordc.contributor.authorVerdejo, Hugo E. es_CL
Authordc.contributor.authorContreras Ferrat, Ariel Eduardo es_CL
Authordc.contributor.authorTroncoso Cotal, Rodrigo es_CL
Authordc.contributor.authorChiong Lay, Mario es_CL
Authordc.contributor.authorLavandero González, Sergio es_CL
Cita de ítemdc.identifier.citationAm J Physiol Endocrinol Metab 306: E1–E13, 2014en_US
General notedc.descriptionArtículo de publicación ISIen_US
Abstractdc.description.abstractInsulin is a major regulator of glucose metabolism, stimulating its mitochondrial oxidation in skeletal muscle cells. Mitochondria are dynamic organelles that can undergo structural remodeling in order to cope with these everchanging metabolic demands. However, the process by which mitochondrial morphology impacts insulin signaling in the skeletal muscle cells remains uncertain. To address this question, we silenced the mitochondrial fusion proteins Mfn2 and Opa1 and assessed insulin-dependent responses in L6 rat skeletal muscle cells. We found that mitochondrial fragmentation attenuates insulin-stimulated Akt phosphorylation, glucose uptake and cell respiratory rate. Importantly, we found that insulin induces a transient rise in mitochondrial Ca2+ uptake, which was attenuated by silencing Opa1 or Mfn2. Moreover, treatment with Ruthenium red, an inhibitor of mitochondrial Ca2+ uptake, impairs Akt signaling without affecting mitochondrial dynamics. All together, these results suggest that control of mitochondrial Ca2 uptake by mitochondrial morphology is a key event for insulininduced glucose uptake.en_US
Patrocinadordc.description.sponsorshipThis work was supported by FONDECYT (Grant 1120212 to S. Lavandero, 3110114 to R. Troncoso, 1110180 to M. Chiong, and 3110170 to A. Contreras- Ferrat), CONICYT (Grant Anillo ACT1111 to S. Lavandero and M. Chiong), and FONDAP (Grant 15130011 to S. Lavandero). We are thankful for the PhD and MSc fellowships from CONICYT Chile to A. del Campo, V. Parra, H. E. Verdejo, P. E. Morales, R. Bravo-Sagua, M. F. Navarro-Marquez, and C. López-Crisosto. V. Parra holds a postdoctoral international fellowship from Bicentennial Program, CONICYT, Chile.en_US
Publisherdc.publisherAmerican Physiological Societyen_US
Type of licensedc.rightsAttribution-NonCommercial-NoDerivs 3.0 Chile*
Link to Licensedc.rights.uri*
Keywordsdc.subjectmitochondrial fragmentationen_US
Títulodc.titleMitochondrial fragmentation impairs insulin-dependent glucose uptake by modulating Akt activity through mitochondrial Ca2+ uptakeen_US
Document typedc.typeArtículo de revistaen_US

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Except where otherwise noted, this item's license is described as Attribution-NonCommercial-NoDerivs 3.0 Chile