PMID- 26281715
OWN - NLM
STAT- MEDLINE
DCOM- 20170501
LR  - 20181113
IS  - 1873-2402 (Electronic)
IS  - 0006-3223 (Print)
IS  - 0006-3223 (Linking)
VI  - 79
IP  - 11
DP  - 2016 Jun 1
TI  - Low Dopamine D2 Receptor Increases Vulnerability to Obesity Via Reduced Physical 
      Activity, Not Increased Appetitive Motivation.
PG  - 887-97
LID - S0006-3223(15)00597-1 [pii]
LID - 10.1016/j.biopsych.2015.07.009 [doi]
AB  - BACKGROUND: The 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. METHODS: We generated a D2R 
      knockdown (KD) mouse line and assessed both energy expenditure and appetitive 
      motivation under conditions of diet-induced obesity. RESULTS: The 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. CONCLUSIONS: These data suggest the primary contribution 
      of altered D2R signaling to obesity lies in altered energy expenditure rather 
      than the induction of compulsive overeating.
CI  - Copyright (c) 2016 Society of Biological Psychiatry. Published by Elsevier Inc. All 
      rights reserved.
FAU - Beeler, Jeff A
AU  - Beeler JA
AD  - Department 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.
FAU - Faust, Rudolf P
AU  - Faust RP
AD  - Interdisciplinary Scientist Training Program, Chicago, Illinois.
FAU - Turkson, Susie
AU  - Turkson S
AD  - Department of Neurobiology (JAB, ST, XZ), Chicago, Illinois.
FAU - Ye, Honggang
AU  - Ye H
AD  - Department of Medicine (HY), University of Chicago, Chicago, Illinois.
FAU - Zhuang, Xiaoxi
AU  - Zhuang X
AD  - Department of Neurobiology (JAB, ST, XZ), Chicago, Illinois.
LA  - eng
GR  - P30 DK020595/DK/NIDDK NIH HHS/United States
GR  - P60 DK020595/DK/NIDDK NIH HHS/United States
GR  - R01 DA025875/DA/NIDA NIH HHS/United States
GR  - R56 DK088515/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20150726
PL  - United States
TA  - Biol Psychiatry
JT  - Biological psychiatry
JID - 0213264
RN  - 0 (Blood Glucose)
RN  - 0 (DRD2 protein, mouse)
RN  - 0 (Receptors, Dopamine D2)
SB  - IM
CIN - Biol Psychiatry. 2016 Jun 1;79(11):e85-6. PMID: 27198522
MH  - Animals
MH  - Blood Glucose
MH  - Body Weight
MH  - Calorimetry, Indirect
MH  - Choice Behavior/physiology
MH  - Conditioning, Operant/physiology
MH  - Disease Models, Animal
MH  - Energy Metabolism/physiology
MH  - Feeding Behavior/*physiology
MH  - Female
MH  - Genetic Predisposition to Disease
MH  - Housing, Animal
MH  - Male
MH  - Mice, 129 Strain
MH  - Mice, Inbred C57BL
MH  - Mice, Transgenic
MH  - Motivation/*physiology
MH  - Motor Activity/*physiology
MH  - Obesity/*metabolism/psychology
MH  - Receptors, Dopamine D2/genetics/*metabolism
PMC - PMC4728060
MID - NIHMS716172
OTO - NOTNLM
OT  - Behavioral thrift
OT  - D(2)R
OT  - Dietary induced obesity
OT  - Reward deficiency
OT  - Running wheels
OT  - Voluntary exercise
EDAT- 2015/08/19 06:00
MHDA- 2017/05/02 06:00
PMCR- 2017/06/01
CRDT- 2015/08/19 06:00
PHST- 2014/11/12 00:00 [received]
PHST- 2015/07/15 00:00 [revised]
PHST- 2015/07/16 00:00 [accepted]
PHST- 2015/08/19 06:00 [entrez]
PHST- 2015/08/19 06:00 [pubmed]
PHST- 2017/05/02 06:00 [medline]
PHST- 2017/06/01 00:00 [pmc-release]
AID - S0006-3223(15)00597-1 [pii]
AID - 10.1016/j.biopsych.2015.07.009 [doi]
PST - ppublish
SO  - Biol Psychiatry. 2016 Jun 1;79(11):887-97. doi: 10.1016/j.biopsych.2015.07.009. 
      Epub 2015 Jul 26.