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