Document Detail


Leptin regulates energy balance and motivation through action at distinct neural circuits.
MedLine Citation:
PMID:  21035790     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
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:
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:
Title:  Biological psychiatry     Volume:  69     ISSN:  1873-2402     ISO Abbreviation:  Biol. Psychiatry     Publication Date:  2011 Apr 
Date Detail:
Created Date:  2011-03-14     Completed Date:  2011-07-01     Revised Date:  2014-09-14    
Medline Journal Info:
Nlm Unique ID:  0213264     Medline TA:  Biol Psychiatry     Country:  United States    
Other Details:
Languages:  eng     Pagination:  668-74     Citation Subset:  IM    
Copyright Information:
Copyright © 2011 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
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:
DK066223/DK/NIDDK NIH HHS; DK40963/DK/NIDDK NIH HHS; R01 DK040963/DK/NIDDK NIH HHS; R01 DK040963-12A1/DK/NIDDK NIH HHS; R01 DK066223-03/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
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; VTD58H1Z2X/Dopamine
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Searching for neuropathology: gliosis in schizophrenia.
Next Document:  The parent-of-origin of the extra X chromosome may differentially affect psychopathology in Klinefel...