Basal Ganglia Dysfunction Contributes to Physical Inactivity in Obesity

Autor: Veronica A. Alvarez, Kevin D. Hall, Alexxai V. Kravitz, Danielle M. Friend, Jeih-San Liow, Marcelo Rubinstein, Sushil G. Rane, Kavya Devarakonda, Ioannis Papazoglou, Alanna R Kaplan, Miguel Skirzewski, Juen Guo, Timothy J. O’Neal
Rok vydání: 2017
Předmět:
Male
0301 basic medicine
Physiology
Dopamine
Action Potentials
Mice
Obese

Striatum
Weight Gain
Obese
Basal Ganglia
purl.org/becyt/ford/1 [https]
0302 clinical medicine
Weight loss
Receptor
Neurons
D2
medicine.symptom
CIENCIAS NATURALES Y EXACTAS
Protein Binding
medicine.drug
medicine.medical_specialty
Movement
Otras Ciencias Biológicas
Motor Activity
Diet
High-Fat

Medium spiny neuron
Article
Ciencias Biológicas
03 medical and health sciences
Physical Conditioning
Animal

Internal medicine
Dopamine receptor D2
Weight Loss
medicine
Animals
Humans
Obesity
purl.org/becyt/ford/1.6 [https]
Exercise
Molecular Biology
Receptors
Dopamine D2

business.industry
Physical Activity
Cell Biology
medicine.disease
Corpus Striatum
Mice
Inbred C57BL

030104 developmental biology
Endocrinology
business
Weight gain
030217 neurology & neurosurgery
Zdroj: CONICET Digital (CONICET)
Consejo Nacional de Investigaciones Científicas y Técnicas
instacron:CONICET
ISSN: 1550-4131
Popis: 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. Fil: Friend, Danielle M.. National Institutes of Health; Estados Unidos Fil: Devarakonda, Kavya. National Institutes of Health; Estados Unidos Fil: O'Neal, Timothy J.. National Institutes of Health; Estados Unidos Fil: Skirzewski, Miguel. National Institutes of Health; Estados Unidos Fil: Papageorgiou, Ioannis. National Institutes of Health; Estados Unidos Fil: Kaplan, Alanna R.. National Institutes of Health; Estados Unidos Fil: Liow, Jeih San. National Institutes of Health; Estados Unidos Fil: Guo, Juen. National Institutes of Health; Estados Unidos Fil: Rane, Sushil G.. National Institutes of Health; Estados Unidos Fil: Rubinstein, Marcelo. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Fisiología, Biología Molecular y Celular; Argentina. University of Michigan; Estados Unidos Fil: Alvarez, Verónica A.. National Institutes of Health; Estados Unidos Fil: Hall, Kevin D.. National Institutes of Health; Estados Unidos Fil: Kravitz, Alexxai V.. National Institutes of Health; Estados Unidos
Databáze: OpenAIRE