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Control of Eating Behavior Using a Novel Feedback System
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La dopamina cerebral y la obesidad.

G J Wang1, N D Volkow, J Logan

  • 1Department of Medicine, Brookhaven National Laboratory, Upton, New York 11973, USA. giwang@bnl.gov

Lancet (London, England)
|February 24, 2001
PubMed
Resumen

Las personas obesas tienen una menor disponibilidad de receptores de dopamina D2, lo que se correlaciona con un IMC más alto. Esta deficiencia de dopamina puede conducir a comer en exceso como un mecanismo de compensación por la activación reducida del circuito de recompensa.

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Área de la Ciencia:

  • La neurociencia es la neurociencia.
  • Trastornos metabólicos Los trastornos metabólicos son trastornos metabólicos que se producen en el cuerpo.
  • Investigación de adicciones Investigación de adicciones.

Sus antecedentes:

  • Los mecanismos patológicos de comer en exceso y la obesidad son poco conocidos.
  • La neurotransmisión de la dopamina está implicada en la recompensa de los alimentos.
  • Investigar la disponibilidad del receptor de dopamina D2 en la obesidad es crucial.

Objetivo del estudio:

  • Para probar la hipótesis de la actividad anormal de dopamina en el cerebro en individuos obesos.
  • Para medir la disponibilidad del receptor de dopamina D2 en el cerebro de individuos obesos y controles.

Principales métodos:

  • La tomografía por emisión de positrones (PET) con [C-11]racloprida se utilizó para medir la disponibilidad del receptor de dopamina D2.
  • La disponibilidad del receptor de dopamina D2 se cuantificó utilizando Bmax/Kd en el estriado.
  • El metabolismo de la glucosa cerebral fue evaluado utilizando 2-deoxy-2[18F]fluoro-D-glucosa (FDG).

Principales resultados:

  • Los individuos obesos mostraron una disponibilidad de los receptores de dopamina D2 estriatal significativamente menor en comparación con los controles.
  • Se encontró una correlación negativa entre el índice de masa corporal (IMC) y la disponibilidad del receptor de dopamina D2 en individuos obesos.
  • No se observaron diferencias en el metabolismo del cerebro entero o del estriado entre los grupos, lo que descarta problemas sistemáticos de entrega de radiotrazadores.

Conclusiones:

  • La disminución de la disponibilidad del receptor de dopamina D2 en individuos obesos es proporcional a su IMC.
  • La deficiencia de dopamina puede perpetuar la alimentación patológica para compensar la activación reducida del circuito de recompensa.
  • Las estrategias terapéuticas dirigidas a la función de la dopamina podrían ayudar en el tratamiento de la obesidad.