Document Detail


Voluntary exercise improves high-fat diet-induced leptin resistance independent of adiposity.
MedLine Citation:
PMID:  21586558     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The efficacy of exercise as primary prevention of obesity is the subject of intense investigation. Here, we show that voluntary exercise in a mouse strain susceptible to diet-induced obesity (C57B6J) decreases fat mass and increases energy expenditure. In addition, exercise attenuates obesity in mice fed a high-fat diet (HFD). Using FosB immunoreactivity as a marker of chronic neuronal activation, we found that exercise activates leptin receptor-positive neurons in the ventromedial hypothalamic nucleus, involved in homeostatic control of energy balance. FosB immunoreactivity in the ventromedial hypothalamic nucleus is decreased in sedentary mice exposed to HFD but is increased in exercised mice independent of adiposity. To determine whether the antiobesity effects of voluntary exercise improve central nervous system (CNS) leptin action, we measured the anorectic and weight reducing effects of intracerebroventricular (ICV) leptin in sedentary and exercised mice exposed to HFD (EH), as well as in sedentary mice that have been calorie restricted (SR) to match the fat mass of EH mice. ICV leptin was ineffective in lowering food intake and body weight (BW) in sedentary mice exposed to HFD mice. The anorectic potency of leptin was partially restored in EH and SR groups. However, ICV leptin significantly lowered BW in EH but not SR mice. Thus, exercise leads to the maintenance of a lower BW and leaner composition, as well as to improved CNS leptin action, independent of fat mass. These results support the notion that physical exercise directly influences the responsiveness of the CNS circuits involved in energy homeostasis by allowing the defense of a lowered BW.
Authors:
Kimberly A Krawczewski Carhuatanta; Giovanna Demuro; Matthias H Tschöp; Paul T Pfluger; Stephen C Benoit; Silvana Obici
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2011-05-17
Journal Detail:
Title:  Endocrinology     Volume:  152     ISSN:  1945-7170     ISO Abbreviation:  Endocrinology     Publication Date:  2011 Jul 
Date Detail:
Created Date:  2011-06-23     Completed Date:  2011-09-02     Revised Date:  2013-06-28    
Medline Journal Info:
Nlm Unique ID:  0375040     Medline TA:  Endocrinology     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2655-64     Citation Subset:  AIM; IM    
Affiliation:
Metabolic Disease Institute and Department of Medicine, College of Medicine, University of Cincinnati, Cincinnati, Ohio 45237-1625, USA.
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MeSH Terms
Descriptor/Qualifier:
Adiposity*
Animals
Appetite Regulation
Caloric Restriction
Dietary Fats / adverse effects*
Energy Metabolism*
Genes, Reporter
Injections, Intraventricular
Leptin / administration & dosage,  metabolism*
Male
Mice
Mice, Inbred C57BL
Mice, Transgenic
Motor Activity*
Nerve Tissue Proteins / metabolism
Neurons / metabolism
Obesity / prevention & control*
Proto-Oncogene Proteins c-fos / metabolism
Random Allocation
Receptors, Leptin / genetics,  metabolism*
Ventromedial Hypothalamic Nucleus / cytology,  physiology
Weight Loss
Grant Support
ID/Acronym/Agency:
DK078283/DK/NIDDK NIH HHS; DK59630/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Dietary Fats; 0/Fosb protein, mouse; 0/Leptin; 0/Nerve Tissue Proteins; 0/Proto-Oncogene Proteins c-fos; 0/Receptors, Leptin; 0/leptin receptor, mouse
Comments/Corrections

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


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