Document Detail


Lipopolysaccharide (LPS) stimulates adipokine and socs3 gene expression in mouse brain and pituitary gland in vivo, and in N-1 hypothalamic neurons in vitro.
MedLine Citation:
PMID:  19261336     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Adipokines that modulate metabolic and inflammatory responses, such as resistin (rstn) and fasting-induced adipose factor (fiaf), are also expressed in mouse brain and pituitary gland. Since lipopolysaccharide (LPS)-induced endotoxinemia provokes an anorectic response via a hypothalamic-dependent mechanism we hypothesized that LPS would also modify hypothalamic adipokine expression. Challenging male CD-1 mice with LPS (5 mg/kg; s.c.) significantly reduced bodyweight (24 h) and realtime RT-PCR revealed time- and tissue-dependent increases in rstn, fiaf and suppressor of cytokine signaling-3 (socs-3) mRNA in hypothalamic, pituitary, cortical and adipose tissues. Gene expression was rapidly increased (3-6 h) in the hypothalamus and pituitary, but returned to normal within 24 h. In contrast, with the exception of rstn in fat, the expression of target genes remained elevated in cortex and visceral fat at 24 h post-injection. In order to more specifically examine the hypothalamic response to LPS we investigated its effects directly on N-1 hypothalamic neurons in vitro. LPS (25 microg/mL; 3 h) had no effect on rstn mRNA, but significantly stimulated fiaf and socs-3 expression. Although various toll-like receptor 4 (TLR4) antagonists (parthenolide, PD098059, and SB202190) did not prevent the LPS-induced increases in fiaf and socs-3, they did partially attenuate its stimulatory effects. We conclude that LPS treatment increases the expression of central, and possibly neuronal, adipokine genes which may influence local tissue repair and function, but could also have downstream consequences on the hypothalamic control of appetite and energy metabolism following an inflammatory insult.
Authors:
Russell Brown; Syed A Imran; Michael Wilkinson
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-03-03
Journal Detail:
Title:  Journal of neuroimmunology     Volume:  209     ISSN:  1872-8421     ISO Abbreviation:  J. Neuroimmunol.     Publication Date:  2009 Apr 
Date Detail:
Created Date:  2009-04-21     Completed Date:  2009-06-22     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8109498     Medline TA:  J Neuroimmunol     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  96-103     Citation Subset:  IM    
Affiliation:
Department of Obstetrics and Gynaecology, Faculty of Medicine, Dalhousie University, c/o IWK Health Centre, Nova Scotia, Canada. Brownre@dal.ca
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MeSH Terms
Descriptor/Qualifier:
Adipokines / genetics*
Adipose Tissue / drug effects,  metabolism,  physiopathology
Angiopoietins / genetics
Animals
Body Weight / drug effects,  physiology
Brain / drug effects,  metabolism*,  physiopathology
Cell Line
Cells, Cultured
Cerebral Cortex / drug effects,  metabolism,  physiopathology
Encephalitis / chemically induced,  metabolism*,  physiopathology
Gene Expression Regulation / drug effects
Hypothalamus / drug effects,  metabolism,  physiopathology
Inflammation Mediators / pharmacology
Lipopolysaccharides / pharmacology
Male
Mice
Neurons / drug effects,  metabolism
Pituitary Gland / drug effects,  metabolism*,  physiopathology
RNA, Messenger / drug effects,  metabolism
Resistin / genetics
Suppressor of Cytokine Signaling Proteins / genetics*
Toll-Like Receptor 4 / antagonists & inhibitors,  metabolism
Chemical
Reg. No./Substance:
0/Adipokines; 0/Angiopoietins; 0/Angptl4 protein, mouse; 0/Inflammation Mediators; 0/Lipopolysaccharides; 0/RNA, Messenger; 0/Resistin; 0/Retn protein, mouse; 0/Socs3 protein, mouse; 0/Suppressor of Cytokine Signaling Proteins; 0/Tlr4 protein, mouse; 0/Toll-Like Receptor 4

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