Basal Ganglia Dysfunction Contributes to Physical Inactivity in Obesity

Obesity is associated with physical inactivity, which exacerbates the health consequences of weight gain. However, the mechanisms that mediate this association are unknown. We hypothesized that deficits in dopamine signaling contribute to physical inactivity in obesity. To investigate this, we quant...

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Autor principal:	Rubinstein, Marcelo
Publicado:	2017
Materias:	D2 dopamine exercise obese obesity physical activity striatum weight loss dopamine 2 receptor protein binding animal experiment animal model Article basal ganglion controlled study corpus striatum diet induced obesity mouse nerve cell nonhuman physical inactivity priority journal signal transduction weight gain action potential adverse effects animal C57BL mouse lipid diet male metabolism mouse mutant movement (physiology) pathophysiology physiology Action Potentials Animals Basal Ganglia Corpus Striatum Diet, High-Fat Male Mice, Inbred C57BL Mice, Obese Movement Neurons Obesity Physical Conditioning, Animal Protein Binding Receptors, Dopamine D2 Weight Gain
Acceso en línea:	https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_15504131_v25_n2_p312_Friend http://hdl.handle.net/20.500.12110/paper_15504131_v25_n2_p312_Friend
Aporte de:	Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) de Universidad de Buenos Aires

id	paper:paper_15504131_v25_n2_p312_Friend
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spelling	paper:paper_15504131_v25_n2_p312_Friend2023-06-08T16:21:33Z Basal Ganglia Dysfunction Contributes to Physical Inactivity in Obesity Rubinstein, Marcelo D2 dopamine exercise obese obesity physical activity striatum weight loss dopamine dopamine 2 receptor protein binding animal experiment animal model Article basal ganglion controlled study corpus striatum diet induced obesity mouse nerve cell nonhuman physical inactivity priority journal signal transduction weight gain action potential adverse effects animal animal experiment basal ganglion C57BL mouse lipid diet male metabolism mouse mutant movement (physiology) obesity pathophysiology physiology Action Potentials Animals Basal Ganglia Corpus Striatum Diet, High-Fat Male Mice, Inbred C57BL Mice, Obese Movement Neurons Obesity Physical Conditioning, Animal Protein Binding Receptors, Dopamine D2 Weight Gain Obesity is associated with physical inactivity, which exacerbates the health consequences of weight gain. However, the mechanisms that mediate this association are unknown. We hypothesized that deficits in dopamine signaling contribute to physical inactivity in obesity. To investigate this, we quantified multiple aspects of dopamine signaling in lean and obese mice. We found that D2-type receptor (D2R) binding in the striatum, but not D1-type receptor binding or dopamine levels, was reduced in obese mice. Genetically removing D2Rs from striatal medium spiny neurons was sufficient to reduce motor activity in lean mice, whereas restoring Gi signaling in these neurons increased activity in obese mice. Surprisingly, although mice with low D2Rs were less active, they were not more vulnerable to diet-induced weight gain than control mice. We conclude that deficits in striatal D2R signaling contribute to physical inactivity in obesity, but inactivity is more a consequence than a cause of obesity. © 2017 Fil:Rubinstein, M. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. 2017 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_15504131_v25_n2_p312_Friend http://hdl.handle.net/20.500.12110/paper_15504131_v25_n2_p312_Friend
institution	Universidad de Buenos Aires
institution_str	I-28
repository_str	R-134
collection	Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
topic	D2 dopamine exercise obese obesity physical activity striatum weight loss dopamine dopamine 2 receptor protein binding animal experiment animal model Article basal ganglion controlled study corpus striatum diet induced obesity mouse nerve cell nonhuman physical inactivity priority journal signal transduction weight gain action potential adverse effects animal animal experiment basal ganglion C57BL mouse lipid diet male metabolism mouse mutant movement (physiology) obesity pathophysiology physiology Action Potentials Animals Basal Ganglia Corpus Striatum Diet, High-Fat Male Mice, Inbred C57BL Mice, Obese Movement Neurons Obesity Physical Conditioning, Animal Protein Binding Receptors, Dopamine D2 Weight Gain
spellingShingle	D2 dopamine exercise obese obesity physical activity striatum weight loss dopamine dopamine 2 receptor protein binding animal experiment animal model Article basal ganglion controlled study corpus striatum diet induced obesity mouse nerve cell nonhuman physical inactivity priority journal signal transduction weight gain action potential adverse effects animal animal experiment basal ganglion C57BL mouse lipid diet male metabolism mouse mutant movement (physiology) obesity pathophysiology physiology Action Potentials Animals Basal Ganglia Corpus Striatum Diet, High-Fat Male Mice, Inbred C57BL Mice, Obese Movement Neurons Obesity Physical Conditioning, Animal Protein Binding Receptors, Dopamine D2 Weight Gain Rubinstein, Marcelo Basal Ganglia Dysfunction Contributes to Physical Inactivity in Obesity
topic_facet	D2 dopamine exercise obese obesity physical activity striatum weight loss dopamine dopamine 2 receptor protein binding animal experiment animal model Article basal ganglion controlled study corpus striatum diet induced obesity mouse nerve cell nonhuman physical inactivity priority journal signal transduction weight gain action potential adverse effects animal animal experiment basal ganglion C57BL mouse lipid diet male metabolism mouse mutant movement (physiology) obesity pathophysiology physiology Action Potentials Animals Basal Ganglia Corpus Striatum Diet, High-Fat Male Mice, Inbred C57BL Mice, Obese Movement Neurons Obesity Physical Conditioning, Animal Protein Binding Receptors, Dopamine D2 Weight Gain
description	Obesity is associated with physical inactivity, which exacerbates the health consequences of weight gain. However, the mechanisms that mediate this association are unknown. We hypothesized that deficits in dopamine signaling contribute to physical inactivity in obesity. To investigate this, we quantified multiple aspects of dopamine signaling in lean and obese mice. We found that D2-type receptor (D2R) binding in the striatum, but not D1-type receptor binding or dopamine levels, was reduced in obese mice. Genetically removing D2Rs from striatal medium spiny neurons was sufficient to reduce motor activity in lean mice, whereas restoring Gi signaling in these neurons increased activity in obese mice. Surprisingly, although mice with low D2Rs were less active, they were not more vulnerable to diet-induced weight gain than control mice. We conclude that deficits in striatal D2R signaling contribute to physical inactivity in obesity, but inactivity is more a consequence than a cause of obesity. © 2017
author	Rubinstein, Marcelo
author_facet	Rubinstein, Marcelo
author_sort	Rubinstein, Marcelo
title	Basal Ganglia Dysfunction Contributes to Physical Inactivity in Obesity
title_short	Basal Ganglia Dysfunction Contributes to Physical Inactivity in Obesity
title_full	Basal Ganglia Dysfunction Contributes to Physical Inactivity in Obesity
title_fullStr	Basal Ganglia Dysfunction Contributes to Physical Inactivity in Obesity
title_full_unstemmed	Basal Ganglia Dysfunction Contributes to Physical Inactivity in Obesity
title_sort	basal ganglia dysfunction contributes to physical inactivity in obesity
publishDate	2017
url	https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_15504131_v25_n2_p312_Friend http://hdl.handle.net/20.500.12110/paper_15504131_v25_n2_p312_Friend
work_keys_str_mv	AT rubinsteinmarcelo basalgangliadysfunctioncontributestophysicalinactivityinobesity
_version_	1768544929911406592

Basal Ganglia Dysfunction Contributes to Physical Inactivity in Obesity

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