Genetic deletion in uncoupling protein 3 augments 18F-fluorodeoxyglucose cardiac uptake in the ischemic heart

BMC Cardiovascular Disorders

Research Article

Giovanni Esposito¹  Alberto Cuocolo¹  Maria Piera Petretta¹  Gabriele G Schiattarella¹  Arturo Brunetti²  Adelaide Greco²  Sara Gargiulo³  Matteo Gramanzini³  Mario Petretta⁴  Michele Larobina⁵  Mariarosaria Panico⁵ 

[1] Department of Advanced Biomedical Sciences, University Federico II, Via Pansini 5, 80131, Naples, Italy;Department of Advanced Biomedical Sciences, University Federico II, Via Pansini 5, 80131, Naples, Italy;CEINGE Scarl, Naples, Italy;Department of Advanced Biomedical Sciences, University Federico II, Via Pansini 5, 80131, Naples, Italy;CEINGE Scarl, Naples, Italy;Institute of Biostructure and Bioimaging, National Council of Research, Naples, Italy;Department of Translational Medical Sciences, University Federico II, Naples, Italy;Institute of Biostructure and Bioimaging, National Council of Research, Naples, Italy;

关键词: Uncoupling protein;    Myocardial infarction;    Glucose metabolism;    Positron emission tomography;   

DOI  :  10.1186/1471-2261-14-98

 received in 2014-04-30, accepted in 2014-07-30,  发布年份 2014

来源: Springer

【 摘 要 】

BackgroundWe investigated the effects of uncoupling protein 3 (UCP3) genetic deletion on 18F-fluorodeoxyglucose (FDG) cardiac uptake by positron emission tomography (PET)/computed tomography (CT) dedicated animal system after permanent coronary artery ligation.MethodsCardiac 18F-FDG PET/CT was performed in UCP3 knockout (UCP3-/-) and wild-type (WT) mice one week after induction of myocardial infarction or sham procedure.ResultsIn sham-operated mice no difference in left ventricular (LV) volume was detectable between WT and UCP3-/-. After myocardial infarction, LV volume was higher in both WT and UCP3-/- compared to sham animals, with a significant interaction (p < 0.05) between genotype and myocardial infarction. In sham-operated animals no difference in FDG standardized uptake value (SUV) was detectable between WT (1.8 ± 0.6) and UCP3-/- (1.8 ± 0.6). After myocardial infarction SUV was significantly higher in remote areas than in infarcted territories in both UCP3-/- and WT mice (both p < 0.01). Moreover, in remote areas, SUV was significantly higher (p < 0.001) in UCP3-/- as compared to WT, while in the infarcted territory SUV was comparable (p = 0.29). A significant relationship (r = 0.68, p < 0.001) between LV volume and SUV was found.ConclusionsIn a mice model of permanent coronary occlusion, UCP3 deficiency results in a metabolic shift that favored glycolytic metabolism and increased FDG uptake in remote areas.

【 授权许可】

Unknown   
© Gargiulo et al.; licensee BioMed Central Ltd. 2014. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.