| Leptin regulates energy balance and motivation through action at distinct neural circuits. | |
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MedLine Citation:
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PMID: 21035790 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND: Overconsumption of calorically dense foods contributes substantially to the current obesity epidemic. The adiposity hormone leptin has been identified as a potential modulator of reward-induced feeding. The current study asked whether leptin signaling within the lateral hypothalamus (LH) and midbrain is involved in effort-based responding for food rewards and/or the modulation of mesolimbic dopamine. METHODS: The contribution of endogenous leptin signaling for food motivation and mesolimbic dopamine tone was examined after viral-mediated reduction of the leptin receptor within LH and midbrain neurons in male rats. RESULTS: Knockdown of leptin receptors selectively in the LH caused increased body weight, caloric consumption, and body fat in rats maintained on a calorically dense diet. Knockdown of leptin receptors selectively in midbrain augmented progressive ratio responding for sucrose and restored high-fat, diet-induced suppression of dopamine content in the nucleus accumbens. CONCLUSIONS: In summary, endogenous leptin signaling in the hypothalamus restrains the overconsumption of calorically dense foods and the consequent increase in body mass, whereas leptin action in the midbrain regulates effort-based responding for food rewards and mesolimbic dopamine tone. These data highlight the ability of leptin to regulate overconsumption of palatable foods and food motivation through pathways that mediate energy homeostasis and reward, respectively. |
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Authors:
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Jon F Davis; Derrick L Choi; Jennifer D Schurdak; Maureen F Fitzgerald; Deborah J Clegg; Jack W Lipton; Dianne P Figlewicz; Stephen C Benoit |
Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S. Date: 2010-10-29 |
Journal Detail:
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Title: Biological psychiatry Volume: 69 ISSN: 1873-2402 ISO Abbreviation: Biol. Psychiatry Publication Date: 2011 Apr |
Date Detail:
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Created Date: 2011-03-14 Completed Date: 2011-07-01 Revised Date: 2012-09-18 |
Medline Journal Info:
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Nlm Unique ID: 0213264 Medline TA: Biol Psychiatry Country: United States |
Other Details:
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Languages: eng Pagination: 668-74 Citation Subset: IM |
Copyright Information:
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Copyright © 2011 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved. |
Affiliation:
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Department of Psychiatry and Behavioral Neuroscience, University of Cincinnati, Cincinnati, Ohio 45237-0506, USA. jon.davis@uc.edu |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Body Weight / drug effects Brain / anatomy & histology, drug effects, metabolism* Conditioning, Operant / drug effects Dietary Fats / administration & dosage Dopamine / metabolism Energy Metabolism / drug effects*, physiology Green Fluorescent Proteins / drug effects*, genetics Leptin / pharmacology* Male Motivation / drug effects* Neural Pathways / physiology RNA, Small Interfering / genetics, metabolism Rats Rats, Long-Evans Receptors, Leptin / genetics STAT3 Transcription Factor / metabolism |
| Grant Support | |
ID/Acronym/Agency:
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DK066223/DK/NIDDK NIH HHS; DK40963/DK/NIDDK NIH HHS; R01 DK040963-12A1/DK/NIDDK NIH HHS; R01 DK040963-24/DK/NIDDK NIH HHS; R01 DK066223-03/DK/NIDDK NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Dietary Fats; 0/Leptin; 0/RNA, Small Interfering; 0/Receptors, Leptin; 0/STAT3 Transcription Factor; 0/Stat3 protein, rat; 147336-22-9/Green Fluorescent Proteins |
| Comments/Corrections | |
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