dc.contributor.author | Guzmán-Ruiz, Rocío | |
dc.contributor.author | Gómez-Hurtado, Nieves | |
dc.contributor.author | Gil-Ortega, Marta | |
dc.contributor.author | Somoza, Beatriz | |
dc.contributor.author | González, Maria Carmen | |
dc.contributor.author | Aránguez, Isabel | |
dc.contributor.author | Martín-Ramos, Miriam | |
dc.contributor.author | González-Martín, Carmen | |
dc.contributor.author | Delgado, Carmen L. | |
dc.contributor.author | Fernández-Alfonso, Marisol S. | |
dc.contributor.author | Ruiz-Gayo, Mariano | |
dc.contributor.other | UAM. Departamento de Fisiología | es_ES |
dc.date.accessioned | 2015-11-16T14:02:03Z | |
dc.date.available | 2015-11-16T14:02:03Z | |
dc.date.issued | 2013-12-18 | |
dc.identifier.citation | Frontiers in Endocrinology 4 (2013): 175 | en_US |
dc.identifier.issn | 1664-2392 | es_ES |
dc.identifier.uri | http://hdl.handle.net/10486/668843 | |
dc.description | This document is protected by copyright and was first published by Frontiers. All rights reserved. it is reproduced with permission | en_US |
dc.description.abstract | Dietary treatment with high-fat diets (HFD) triggers diabetes and hyperleptinemia, concomitantly
with a partial state of leptin resistance that affects hepatic and adipose tissue
but not the heart. In this context, characterized by widespread steatosis, cardiac lipid content
remains unchanged. As previously reported, HFD-evoked hyperleptinemia could be a
pivotal element contributing to increase fatty-acid (FA) metabolism in the heart and to
prevent cardiac steatosis. This metabolic adaptation might theoretically reduce energy
efficiency in cardiomyocytes and lead to cardiac electrophysiological remodeling. Therefore
the aim of the current study has been to investigate the impact of long-term HFD
on cardiac metabolism and electrophysiological properties of the principal ionic currents
responsible of the action potential duration in mouse cardiomyocytes. Male C57BL/6J
mice were fed a control (10 kcal% from fat) or HFD (45 kcal% from fat) during 32weeks.
Quantification of enzymatic activities regulating mitochondrial uptake of pyruvate and FA
showed an increase of both carnitine-palmitoyltransferase and citrate synthase activities
together with a decrease of lactate dehydrogenase and pyruvate dehydrogenase activities.
Increased expression of uncoupling protein-3, Mn-, and Cu/Zn-superoxide dismutases and
catalase were also detected. Total glutathione/oxidized glutathione ratios were unaffected
by HFD.These data suggest that HFD triggers adaptive mechanisms aimed at (i) facilitating
FA catabolism, and (ii) preventing oxidative stress. All these changes did not affect the duration
of action potentials in cardiomyocytes and only slightly modified electrocardiographic
parameters | en_US |
dc.description.sponsorship | This work was supported by grants
from Ministerio de Economía y Competitividad (BFU2012-35353,
SAF2008-02703, SAF2010-16377), Fundación Mutua Madrileña
(GR-921641), Fundación Universitaria San Pablo–Ceu, Universidad
Complutense de Madrid (UCMGR-921641), RECAVA
(RD06-0014-007), and SESCAMET | en_US |
dc.format.extent | 9 pag. | en |
dc.format.mimetype | application/pdf | en |
dc.language.iso | eng | en |
dc.publisher | Frontiers Research Foundation | en_US |
dc.relation.ispartof | Frontiers in Endocrinology | en_US |
dc.rights | © 2013 The Authors | en_US |
dc.subject.other | Cardiac metabolism | en_US |
dc.subject.other | Electrophysiology | en_US |
dc.subject.other | Leptin | en_US |
dc.subject.other | Obesity | en_US |
dc.subject.other | UCP3 | en_US |
dc.title | Remodeling of energy metabolism and absence of electrophysiological changes in the heart of obese hyperleptinemic mice. New insights into the pleiotropic role of leptin | en_US |
dc.type | article | en |
dc.subject.eciencia | Medicina | es_ES |
dc.relation.publisherversion | http://dx.doi.org/10.3389/fendo.2013.00175 | es_ES |
dc.identifier.doi | 10.3389/fendo.2013.00175 | es_ES |
dc.identifier.publicationfirstpage | 175-1 | es_ES |
dc.identifier.publicationlastpage | 175-9 | es_ES |
dc.identifier.publicationvolume | 4 | es_ES |
dc.relation.projectID | Gobierno de España. BFU2012-35353 | es_Es |
dc.relation.projectID | Gobierno de España. SAF2008-02703 | es_ES |
dc.relation.projectID | Gobierno de España. SAF2010-16377 | es_ES |
dc.type.version | info:eu-repo/semantics/publishedVersion | en |
dc.rights.cc | Reconocimiento | es_ES |
dc.rights.accessRights | openAccess | en |
dc.facultadUAM | Facultad de Medicina | |