Petretta, Maria Piera (2014) Genetic deletion in Uncoupling Protein 3 augments 18F-Fluorodeoxyglucose cardiac uptake in the ischemic heart. [Tesi di dottorato]

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Item Type: Tesi di dottorato
Lingua: English
Title: Genetic deletion in Uncoupling Protein 3 augments 18F-Fluorodeoxyglucose cardiac uptake in the ischemic heart
Creators:
CreatorsEmail
Petretta, Maria Pieramariapiera.petretta@gmail.com
Date: 18 March 2014
Number of Pages: 47
Institution: Università degli Studi di Napoli Federico II
Department: Scienze Biomediche Avanzate
Scuola di dottorato: Scienze biomorfologiche e chirurgiche
Dottorato: Imaging molecolare
Ciclo di dottorato: 26
Coordinatore del Corso di dottorato:
nomeemail
Salvatore, MarcoUNSPECIFIED
Tutor:
nomeemail
Cuocolo, AlbertoUNSPECIFIED
Date: 18 March 2014
Number of Pages: 47
Uncontrolled Keywords: imaging molecolare; apparato cardiovascolare; PET/TAC
Settori scientifico-disciplinari del MIUR: Area 06 - Scienze mediche > MED/11 - Malattie dell'apparato cardiovascolare
Area 06 - Scienze mediche > MED/36 - Diagnostica per immagini e radioterapia
Date Deposited: 16 Apr 2014 11:20
Last Modified: 15 Jul 2015 01:01
URI: http://www.fedoa.unina.it/id/eprint/9638

Abstract

Background — Uncoupling protein 3 (UCP3) is a member of the mitochondrial anion carrier super-family of proteins expressed in the mitochondrial inner membrane that uncouple oxygen consumption by the respiratory chain from ATP synthesis. UCP3 plays a role in fatty acid metabolism and energy homeostasis and is required to maintain high rates of glucose aerobic metabolism, while deficiency in UCP3 might results in a metabolic shift that promotes anaerobic glycolytic metabolism. In this study, we investigated the effects of UCP3 genetic deletion on 18F-fluorodeoxyglucose (FDG) cardiac uptake by a high-resolution positron emission tomography (PET)/computed tomography (CT) dedicated animal system after permanent coronary artery ligation. Methods and Results — To test the effects of UCP3 genetic deletion in vivo, cardiac 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. 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 higher in both WT (2.2 ± 0.6) and UCP3-/- (4.0 ± 0.9) compared to sham animals, with a significant interaction (P < 0.005) between genotype and myocardial infarction. 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 is required to maintain high rates of glucose aerobic metabolism and its deficiency results in a metabolic shift that favored anaerobic glycolytic metabolism and increased FDG uptake.

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