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 |
|---|---|
| Resource language: | English |
| Title: | Genetic deletion in Uncoupling Protein 3 augments 18F-Fluorodeoxyglucose cardiac uptake in the ischemic heart |
| Creators: | Creators Email Petretta, Maria Piera mariapiera.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: | nome email Salvatore, Marco UNSPECIFIED |
| Tutor: | nome email Cuocolo, Alberto UNSPECIFIED |
| Date: | 18 March 2014 |
| Number of Pages: | 47 |
| 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 |
Collection description
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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