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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

Vertical long-axis, horizontal long-axis, and short-axis slices (on the bottom) and the resulting polar map (on the top) in a WT mouse (A) and an UCP3−/− mouse (B) after myocardial infarction.
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Figure 2: Vertical long-axis, horizontal long-axis, and short-axis slices (on the bottom) and the resulting polar map (on the top) in a WT mouse (A) and an UCP3−/− mouse (B) after myocardial infarction.

Mentions: At trans-thoracic echocardiography, sham-operated UCP3−/− mice showed LV fractional shortening comparable to WT (56.5 ± 4.6% and 54.1 ± 4.2%, respectively, p = NS). After myocardial infarction, LV fractional shortening was significantly lower (p < 0.05) in both WT (42.7 ± 3.1%) and UCP3−/− (24.4 ± 2.5%) mice compared to sham-operated animals. UCP3−/− mice displayed a significant worsening in cardiac function after coronary artery ligation compared with WT (p < 0.05). Furthermore, UCP3 genetic deletion increased infarct size after coronary artery ligation as compared to WT (44 ± 9% vs. 29 ± 7%, p < 0.005). Vertical long-axis, horizontal long-axis, and short-axis slices and the resulting polar map in a WT mouse and an UCP3−/− mouse after myocardial infarction are illustrated in Figure 2.


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)

Vertical long-axis, horizontal long-axis, and short-axis slices (on the bottom) and the resulting polar map (on the top) in a WT mouse (A) and an UCP3−/− mouse (B) after myocardial infarction.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 2: Vertical long-axis, horizontal long-axis, and short-axis slices (on the bottom) and the resulting polar map (on the top) in a WT mouse (A) and an UCP3−/− mouse (B) after myocardial infarction.
Mentions: At trans-thoracic echocardiography, sham-operated UCP3−/− mice showed LV fractional shortening comparable to WT (56.5 ± 4.6% and 54.1 ± 4.2%, respectively, p = NS). After myocardial infarction, LV fractional shortening was significantly lower (p < 0.05) in both WT (42.7 ± 3.1%) and UCP3−/− (24.4 ± 2.5%) mice compared to sham-operated animals. UCP3−/− mice displayed a significant worsening in cardiac function after coronary artery ligation compared with WT (p < 0.05). Furthermore, UCP3 genetic deletion increased infarct size after coronary artery ligation as compared to WT (44 ± 9% vs. 29 ± 7%, p < 0.005). Vertical long-axis, horizontal long-axis, and short-axis slices and the resulting polar map in a WT mouse and an UCP3−/− mouse after myocardial infarction are illustrated in Figure 2.

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