Stimulating the nucleus accumbens in obesity: a positron emission tomography study after deep brain stimulation in a rodent model
Editorial:
PLOS
Fecha de edición:
2018-09-27
Cita:
Casquero-Veiga, et al. Stimulating the nucleus accumbens in obesity: a positron emission tomography study after deep brain stimulation in a rodent model. In: PLoS ONE 13(9): e0204740, Sept. 2018, 14 pp.
ISSN:
1932-6203
Patrocinador:
Comunidad de Madrid
Ministerio de Economía y Competitividad (España)
Plan Nacional sobre Drogas (España)
Ministerio de Economía, Industria y Competitividad (España)
Agradecimientos:
This research was supported by the Ministry of Economy and Competitiveness ISCIII grants (PI14/00860, CPII14/00005), Ministry of Economy, Industry and Competitiveness (PI17/01766), cofunded by ERDF (FEDER) Funds from the European Commission "A way of making Europe", Fundación Mapfre, Fundación Alicia Koplowitz (FAK2016/01), 'Delegación de Gobierno para el Plan Nacional sobre Drogas' (PNSD 2017/085), Comunidad de Madrid (BRADE-CM S2013/ICE-2958) and Fundación Tatiana Pérez de Guzmán el Bueno.
Proyecto:
Gobierno de España. PI14/00860
Gobierno de España. CPII14/00005
Gobierno de España. PI17/01766
Gobierno de España. PNSD 2017/085
Comunidad de Madrid. S2013/ICE-2958
Palabras clave:
Deep brain stimulation
,
Disease models
,
Nucleus accumbens
,
Obesity
,
Positron-emission tomography
,
Diagnostic imaging
,
Rats
,
Zucker rat
Derechos:
© 2018 Casquero-Veiga et al.
This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Atribución 3.0 España
Resumen:
Purpose: The nucleus accumbens (NAcc) has been suggested as a possible target for deep brain stimulation (DBS) in the treatment of obesity. Our hypothesis was that NAcc-DBS would modulate brain regions related to reward and food intake regulation, consequently
Purpose: The nucleus accumbens (NAcc) has been suggested as a possible target for deep brain stimulation (DBS) in the treatment of obesity. Our hypothesis was that NAcc-DBS would modulate brain regions related to reward and food intake regulation, consequently reducing the food intake and, finally, the weight gain. Therefore, we examined changes in brain glucose metabolism, weight gain and food intake after NAcc-DBS in a rat model of obesity. Procedures: Electrodes were bilaterally implanted in 2 groups of obese Zucker rats targeting the NAcc. One group received stimulation one hour daily during 15 days, while the other remained as control. Weight and daily consumption of food and water were everyday registered the days of stimulation, and twice per week during the following month. Positron emission tomography (PET) studies with 2-deoxy-2-[F-18] fluoro-D-glucose (FDG) were performed 1 day after the end of DBS. PET data was assessed by statistical parametric mapping (SPM12) software and region of interest (ROI) analyses. Results: NAcc-DBS lead to increased metabolism in the cingulate-retrosplenial-parietal association cortices, and decreased metabolism in the NAcc, thalamic and pretectal nuclei. Furthermore, ROIs analyses confirmed these results by showing a significant striatal and thalamic hypometabolism, and a cortical hypermetabolic region. However, NAcc-DBS did not induce a decrease in either weight gain or food intake. Conclusions: NAcc-DBS led to changes in the metabolism of regions associated with cognitive and reward systems, whose impairment has been described in obesity.
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