Evidence map›Paper›PMID 26281715›Full record

ArticleBiological psychiatry2016

Low Dopamine D2 Receptor Increases Vulnerability to Obesity Via Reduced Physical Activity, Not Increased Appetitive Motivation.

Jeff A Beeler, Rudolf P Faust, Susie Turkson, Honggang Ye, Xiaoxi Zhuang

Abstract read
In one paragraph

Article in Biological psychiatry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 1 pooled it
13.3field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

44 citing papers in PubMed, 1 synthesis or guideline pooled it, 97 citations in OpenAlex.

  1. Pooled it
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  15. Biological psychiatry global open science · 2023
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  19. High Fat Diet Increases [Neurochemical research · 2022
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Jeff A BeelerDepartment of Psychology, Queens College and the Graduate Center, City University of New York, Flushing, New York; Department of Neurobiology (JAB, ST, XZ), Chicago, Illinois. Electronic address: jbeeler@qc.cuny.edu.
Rudolf P FaustInterdisciplinary Scientist Training Program, Chicago, Illinois.
Susie TurksonDepartment of Neurobiology (JAB, ST, XZ), Chicago, Illinois.
Honggang YeDepartment of Medicine (HY), University of Chicago, Chicago, Illinois.
Xiaoxi ZhuangDepartment of Neurobiology (JAB, ST, XZ), Chicago, Illinois.
Queens College, CUNY · USUniversity of Chicago · US

Funding

TRANSGENIC COREP60DK020595 · NIDDK · UNIVERSITY OF CHICAGO · PI BELL, GRAEME I · 1985 to 2012
$25.5M
Pilot and Feasibility ProgramP30DK020595 · NIDDK · UNIVERSITY OF CHICAGO · PI Matthew J Brady · 2013 to 2026
$20.9M
Pharmacological Targets Facilitating Non-Drug Reward & Extinction of Drug-SeekingR01DA025875 · NIDA · UNIVERSITY OF CHICAGO · PI BEELER, JEFF A. · 2008 to 2012
$1.6M
Reward mechanisms in feeding and obesityR56DK088515 · NIDDK · UNIVERSITY OF CHICAGO · PI ZHUANG, XIAOXI · 2010 to 2010
$385k
NIDA NIH HHS R01 DA025875NIDDK NIH HHS P30 DK020595NIDDK NIH HHS P60 DK020595NIDDK NIH HHS R56 DK088515
6 · The paper itself

Abstract

backgroundThe dopamine D2 receptor (D2R) has received much attention in obesity studies. Data indicate that D2R is reduced in obesity and that the TaqA1 D2R variant may be more prevalent among obese persons. It is often suggested that reduced D2R generates a reward deficiency and altered appetitive motivation that induces compulsive eating and contributes to obesity. Although dopamine is known to regulate physical activity, it is often neglected in these studies, leaving open the question of whether reduced D2R contributes to obesity through alterations in energy expenditure and activity.

methodsWe generated a D2R knockdown (KD) mouse line and assessed both energy expenditure and appetitive motivation under conditions of diet-induced obesity.

resultsThe KD mice did not gain more weight or show increased appetitive motivation compared with wild-type mice in a standard environment; however, in an enriched environment with voluntary exercise opportunities, KD mice exhibited dramatically lower activity and became more obese than wild-type mice, obtaining no protective benefit from exercise opportunities.

conclusionsThese data suggest the primary contribution of altered D2R signaling to obesity lies in altered energy expenditure rather than the induction of compulsive overeating.

Indexed as

AnimalsBlood GlucoseBody WeightCalorimetry, IndirectChoice BehaviorConditioning, OperantDisease Models, AnimalEnergy MetabolismFeeding BehaviorFemaleGenetic Predisposition to DiseaseHousing, AnimalMaleMice, 129 StrainMice, Inbred C57BLMice, TransgenicBlood GlucoseDRD2 protein, mouseReceptors, Dopamine D2Behavioral thriftD(2)RDietary induced obesityReward deficiencyRunning wheelsVoluntary exercise

Identifiers

PMID26281715
PMCPMC4728060
OpenAlexW981533126

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.