Document Detail


A role for central nervous system PPAR-γ in the regulation of energy balance.
MedLine Citation:
PMID:  21532595     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The peroxisome proliferator-activated receptor-γ (PPAR-γ) is a nuclear receptor that is activated by lipids to induce the expression of genes involved in lipid and glucose metabolism, thereby converting nutritional signals into metabolic consequences. PPAR-γ is the target of the thiazolidinedione (TZD) class of insulin-sensitizing drugs, which have been widely prescribed to treat type 2 diabetes mellitus. A common side effect of treatment with TZDs is weight gain. Here we report a previously unknown role for central nervous system (CNS) PPAR-γ in the regulation of energy balance. We found that both acute and chronic activation of CNS PPAR-γ, by either TZDs or hypothalamic overexpression of a fusion protein consisting of PPAR-γ and the viral transcriptional activator VP16 (VP16-PPAR-γ), led to positive energy balance in rats. Blocking the endogenous activation of CNS PPAR-γ with pharmacological antagonists or reducing its expression with shRNA led to negative energy balance, restored leptin sensitivity in high-fat-diet (HFD)-fed rats and blocked the hyperphagic response to oral TZD treatment. These findings have implications for the widespread clinical use of TZD drugs and for understanding the etiology of diet-induced obesity.
Authors:
Karen K Ryan; Bailing Li; Bernadette E Grayson; Emily K Matter; Stephen C Woods; Randy J Seeley
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2011-05-01
Journal Detail:
Title:  Nature medicine     Volume:  17     ISSN:  1546-170X     ISO Abbreviation:  Nat. Med.     Publication Date:  2011 May 
Date Detail:
Created Date:  2011-05-06     Completed Date:  2011-07-05     Revised Date:  2011-11-01    
Medline Journal Info:
Nlm Unique ID:  9502015     Medline TA:  Nat Med     Country:  United States    
Other Details:
Languages:  eng     Pagination:  623-6     Citation Subset:  IM    
Affiliation:
Department of Internal Medicine, Division of Endocrinology, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Blood-Brain Barrier
Central Nervous System / drug effects,  physiology*
Energy Metabolism / physiology*
Gene Expression
Humans
Hypoglycemic Agents / adverse effects,  pharmacology
Hypothalamus / drug effects,  physiology
Male
PPAR gamma / agonists,  antagonists & inhibitors,  genetics,  physiology*
RNA, Small Interfering / genetics
Rats
Rats, Long-Evans
Recombinant Fusion Proteins / genetics
Thiazolidinediones / adverse effects,  pharmacology
Weight Gain / drug effects,  physiology
Grant Support
ID/Acronym/Agency:
DK056863/DK/NIDDK NIH HHS; DK073505/DK/NIDDK NIH HHS; DK082173/DK/NIDDK NIH HHS; DK17844/DK/NIDDK NIH HHS; R01 DK017844-35/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Hypoglycemic Agents; 0/PPAR gamma; 0/RNA, Small Interfering; 0/Recombinant Fusion Proteins; 0/Thiazolidinediones; 122320-73-4/rosiglitazone
Comments/Corrections
Comment In:
Nat Med. 2011 May;17(5):544-5   [PMID:  21546969 ]

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


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