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Brain dopamine and obesity.

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
Summary
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Obese individuals have lower dopamine D2 receptor availability, which correlates with higher BMI. This dopamine deficiency may drive overeating as a compensation mechanism for reduced reward circuit activation.

Area of Science:

  • Neuroscience
  • Metabolic Disorders
  • Addiction Research

Background:

  • Pathological overeating and obesity mechanisms are poorly understood.
  • Dopamine neurotransmission is implicated in food reward.
  • Investigating dopamine D2 receptor availability in obesity is crucial.

Purpose of the Study:

  • To test the hypothesis of abnormal brain dopamine activity in obese individuals.
  • To measure dopamine D2 receptor availability in the brains of obese individuals and controls.

Main Methods:

  • Positron emission tomography (PET) with [C-11]raclopride was used to measure dopamine D2 receptor availability.
  • Dopamine D2 receptor availability was quantified using Bmax/Kd in the striatum.
  • Brain glucose metabolism was assessed using 2-deoxy-2[18F]fluoro-D-glucose (FDG).

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Main Results:

  • Obese individuals showed significantly lower striatal dopamine D2 receptor availability compared to controls.
  • A negative correlation was found between body mass index (BMI) and dopamine D2 receptor availability in obese individuals.
  • No differences in whole brain or striatal metabolism were observed between groups, ruling out systematic radiotracer delivery issues.

Conclusions:

  • Decreased dopamine D2 receptor availability in obese individuals is proportional to their BMI.
  • Dopamine deficiency may perpetuate pathological eating to compensate for reduced reward circuit activation.
  • Therapeutic strategies targeting dopamine function could aid in obesity treatment.