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Completed Not applicable Interventional Accepts healthy volunteers

Brain, Obesity, Dopamine and You Study

ClinicalTrials.gov ID: NCT01094756

Public ClinicalTrials.gov record NCT01094756. Field values are reproduced from the official study page; the official ClinicalTrials.gov record remains the source of truth for eligibility, enrollment, and contact information.

ClinicalTrials.gov public records Last synced Sep 2, 2026, 10:24 AM EDT

Data is sourced from official ClinicalTrials.gov public API records. Always review the official ClinicalTrials.gov record for the latest information.

Official title

Central Dopamine Receptors In Obesity

Brief summary

Reproduced verbatim from the official ClinicalTrials.gov record. Not medical advice.

Central dopamine is thought to play a significant role in obesity. In support of this idea, animal studies and one human positron emission tomography (PET) study have found reduced postsynaptic D2-like receptor availability in the striatum in obesity, with lower D2 receptor availability associated with higher weight. In addition, reward sensitivity and hedonic responses, known to be related to dopamine function, have also been implicated in obesity and obesity-related eating behavior. These reports have led to the concept that dopaminergic abnormalities (e.g. reduced D2-like receptors) influence reward sensitivity, leading to altered eating behaviors and eventually obesity. However, there are several critical limitations of the human D2 receptor studies that limit the strength of their conclusions and thus the interpretations and speculations embedded in literature that relies on this work. First, estimates of D2-like receptors in humans have been confounded by potential differences in endogenous dopamine release since the PET ligand (raclopride) used is known to be displaceable from receptors by endogenous dopamine. Second, failure to rigorously screen obese individuals for diabetes confounds conclusions, since diabetes has been independently associated with dopaminergic abnormalities such as reduced D2-like receptors and muted dopamine release in diabetic rats. Finally, no human studies have addressed whether reduced D2-like receptor levels are a risk factor for obesity, a consequence of engaging in obesity-related behaviors or being obese or all of the above.

Study identification

NCT ID
NCT01094756
Recruitment status
Completed
Study type
Interventional
Phase
Not applicable
Enrollment
82 participants

Conditions and interventions

Conditions

Interventions

Dietary Supplement

Eligibility (public fields only)

Age range
18 Years to 40 Years
Sex
All
Healthy volunteers
Accepts healthy volunteers

This page does not interpret eligibility. Detailed inclusion and exclusion criteria are on the official ClinicalTrials.gov record.

Study timeline

Start date
Jun 30, 2010
Primary completion
May 31, 2015
Completion
Sep 30, 2016
Last update posted
Nov 1, 2016

2010 – 2016

United States locations

U.S. sites
1
U.S. states
1
U.S. cities
1
Facility City State ZIP Site status
Washington University Medical School St Louis Missouri 63110

Site contact phone numbers, emails, and investigator names are intentionally not displayed here. Open the official ClinicalTrials.gov record for site contact information.

About this trial record page

What this page shows
Public field values for ClinicalTrials.gov record NCT01094756, including study identification, conditions, interventions, eligibility (age, sex, healthy volunteer), timeline, and U.S. site list.
What this page does not do
No medical advice, eligibility judgments, treatment recommendations, study quality scoring, or AI-generated medical summaries. No site contact phone numbers, emails, or investigator names.
Where the data comes from
Sourced from the official ClinicalTrials.gov public API. The official record is the source of truth.
Last refresh
Last update posted Nov 1, 2016 · Synced Sep 2, 2026

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Open the official record

The complete protocol, eligibility criteria, and contact information for NCT01094756 live on ClinicalTrials.gov.

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