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

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Item Type:Article
Title:Genetic deletion in uncoupling protein 3 augments (18)F-fluorodeoxyglucose cardiac uptake in the ischemic heart
Creators Name:Gargiulo, S. and Petretta, M.P. and Greco, A. and Panico, M. and Larobina, M. and Gramanzini, M. and Schiattarella, G.G. and Esposito, G. and Petretta, M. and Brunetti, A. and Cuocolo, A.
Abstract:BACKGROUND: We investigated the effects of uncoupling protein 3 (UCP3) genetic deletion on (18)F-fluorodeoxyglucose (FDG) cardiac uptake by positron emission tomography (PET)/computed tomography (CT) dedicated animal system after permanent coronary artery ligation. METHODS: Cardiac (18)F-FDG PET/CT was performed in UCP3 knockout (UCP3(-/-)) and wild-type (WT) mice one week after induction of myocardial infarction or sham procedure. RESULTS: In 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. CONCLUSIONS: In 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.
Keywords:Uncoupling Protein, Myocardial Infarction, Glucose Metabolism, Positron Emission Tomography, Animals, Mice
Source:BMC Cardiovascular Disorders
ISSN:1471-2261
Publisher:BioMed Central
Volume:14
Page Range:98
Date:8 August 2014
Official Publication:https://doi.org/10.1186/1471-2261-14-98
PubMed:View item in PubMed

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