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Updated: Jul 12, 2026
04:48
Control of Eating Behavior Using a Novel Feedback System
Published on: May 8, 2018
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
Summary
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).
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.
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