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

Gargiulo S, Petretta MP, Greco A, Panico M, Larobina M, Gramanzini M, Schiattarella GG, Esposito G, Petretta M, Brunetti A, Cuocolo A - BMC Cardiovasc Disord (2014)

Bottom Line: 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.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.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Advanced Biomedical Sciences, University Federico II, Via Pansini 5, 80131 Naples, Italy. cuocolo@unina.it.

ABSTRACT

Background: We 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.

Methods: 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.

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.

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Related in: MedlinePlus

Individual values for LV volume in sham-operated and myocardial infarction WT and UCP3−/− mice. Closed circles indicate mean ± standard deviation.
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Figure 1: Individual values for LV volume in sham-operated and myocardial infarction WT and UCP3−/− mice. Closed circles indicate mean ± standard deviation.

Mentions: Individual values of LV volume in the four groups of mice are illustrated in Figure 1. In sham-operated mice no difference was detectable between WT (56.1 ± 6.1 μl) and UCP3−/− (58.7 ± 5.1 μl). After myocardial infarction, LV volume was higher in both WT (59.9 ± 9.3 μl) and UCP3−/− (75.5 ± 10.8 μl) as compared to sham animals, with UCP3−/− mice showing the highest values. At two-way analysis of variance a significant interaction (p < 0.05) between genotype and myocardial infarction was found (Table 1).


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

Gargiulo S, Petretta MP, Greco A, Panico M, Larobina M, Gramanzini M, Schiattarella GG, Esposito G, Petretta M, Brunetti A, Cuocolo A - BMC Cardiovasc Disord (2014)

Individual values for LV volume in sham-operated and myocardial infarction WT and UCP3−/− mice. Closed circles indicate mean ± standard deviation.
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4127083&req=5

Figure 1: Individual values for LV volume in sham-operated and myocardial infarction WT and UCP3−/− mice. Closed circles indicate mean ± standard deviation.
Mentions: Individual values of LV volume in the four groups of mice are illustrated in Figure 1. In sham-operated mice no difference was detectable between WT (56.1 ± 6.1 μl) and UCP3−/− (58.7 ± 5.1 μl). After myocardial infarction, LV volume was higher in both WT (59.9 ± 9.3 μl) and UCP3−/− (75.5 ± 10.8 μl) as compared to sham animals, with UCP3−/− mice showing the highest values. At two-way analysis of variance a significant interaction (p < 0.05) between genotype and myocardial infarction was found (Table 1).

Bottom Line: 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.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.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Advanced Biomedical Sciences, University Federico II, Via Pansini 5, 80131 Naples, Italy. cuocolo@unina.it.

ABSTRACT

Background: We 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.

Methods: 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.

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.

Show MeSH
Related in: MedlinePlus