Journal article
A Role for ΔFosB in Calorie Restriction-Induced Metabolic Changes
Biological psychiatry (1969), Vol.70(2), pp.204-207
2011
DOI: 10.1016/j.biopsych.2010.11.027
PMCID: PMC3125466
PMID: 21215388
Abstract
Calorie restriction (CR) induces long-term changes in motivation to eat highly palatable food and, in body weight regulation, through an unknown mechanism.
After a period of CR and refeeding, mice were assessed by behavioral and metabolic studies and for levels of the transcription factor ΔFosB. The ΔFosB levels were then increased specifically in nucleus accumbens (NAc) with viral-mediated gene transfer, and behavioral and metabolic studies were conducted.
We show that accumulation of ΔFosB in the NAc shell after CR in mice corresponds to a period of increased motivation for high fat reward and reduced energy expenditure. Furthermore, ΔFosB overexpression in this region increases instrumental responding for a high fat reward via an orexin-dependent mechanism while also decreasing energy expenditure and promoting adiposity.
These results suggest that ΔFosB signaling in NAc mediates adaptive responses to CR.
Details
- Title: Subtitle
- A Role for ΔFosB in Calorie Restriction-Induced Metabolic Changes
- Creators
- Vincent Vialou - Fishberg Department of Neuroscience, Mount Sinai School of Medicine, New York, New YorkHuxing Cui - Department of Psychiatry, Division of Hypothalamic Research, University of Texas Southwestern Medical Center, Dallas, TexasMario Perello - Department of Internal Medicine, Division of Hypothalamic Research, University of Texas Southwestern Medical Center, Dallas, TexasMelissa Mahgoub - Department of Psychiatry, Division of Hypothalamic Research, University of Texas Southwestern Medical Center, Dallas, TexasHana G Yu - Department of Psychiatry, Division of Hypothalamic Research, University of Texas Southwestern Medical Center, Dallas, TexasAugustus J Rush - Department of Psychiatry, Division of Hypothalamic Research, University of Texas Southwestern Medical Center, Dallas, TexasHeena Pranav - Department of Psychiatry, Division of Hypothalamic Research, University of Texas Southwestern Medical Center, Dallas, TexasSaendy Jung - Department of Psychiatry, Division of Hypothalamic Research, University of Texas Southwestern Medical Center, Dallas, TexasMasashi Yangisawa - Department of Molecular Genetics and the Howard Hughes Medical Institute, Division of Hypothalamic Research, University of Texas Southwestern Medical Center, Dallas, TexasJeffrey M Zigman - Department of Internal Medicine, Division of Hypothalamic Research, University of Texas Southwestern Medical Center, Dallas, TexasJoel K Elmquist - Department of Internal Medicine, Division of Hypothalamic Research, University of Texas Southwestern Medical Center, Dallas, TexasEric J Nestler - Fishberg Department of Neuroscience, Mount Sinai School of Medicine, New York, New YorkMichael Lutter - Department of Psychiatry, Division of Hypothalamic Research, University of Texas Southwestern Medical Center, Dallas, Texas
- Resource Type
- Journal article
- Publication Details
- Biological psychiatry (1969), Vol.70(2), pp.204-207
- Publisher
- Elsevier Inc
- DOI
- 10.1016/j.biopsych.2010.11.027
- PMID
- 21215388
- PMCID
- PMC3125466
- ISSN
- 0006-3223
- eISSN
- 1873-2402
- Grant note
- DOI: 10.13039/100009670, name: National Alliance for Research on Schizophrenia and Depression; name: AstraZeneca; name: The Physician Scientist Training Program; name: The Disease Oriented Clinical Scholars Program; name: Medical Scientist Training Program
- Language
- English
- Date published
- 2011
- Academic Unit
- Iowa Neuroscience Institute; Fraternal Order of Eagles Diabetes Research Center; Neuroscience and Pharmacology
- Record Identifier
- 9984040312402771
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