Linked Life Data

16554545

Source:http://linkedlifedata.com/resource/pubmed/id/16554545

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2006-5-17
pubmed:abstractText
In response to infection or inflammation, individuals develop a set of symptoms referred to as sickness behavior, which includes a decrease in food intake. The characterization of the molecular mechanisms underlying this hypophagia remains critical, because chronic anorexia may represent a significant health risk. Prostaglandins (PGs) constitute an important inflammatory mediator family whose levels increase in the brain during inflammatory states, and their involvement in inflammatory-induced anorexia has been proposed. The microsomal PGE synthase (mPGES)-1 enzyme is involved in the last step of PGE2 biosynthesis, and its expression is stimulated by proinflammatory agents. The present study attempted to determine whether an upregulation of mPGES-1 gene expression may account for the immune-induced anorexic behavior. We focused our study on mPGES-1 expression in the hypothalamus and dorsal vagal complex, two structures strongly activated during peripheral inflammation and involved in the regulation of food intake. We showed that mPGES-1 gene expression was robustly upregulated in these structures after intraperitoneal and intracerebroventricular injections of anorexigenic doses of IL-1beta. This increase was correlated with the onset of anorexia. The concomitant reduction in food intake and central mPGES-1 gene upregulation led us to test the feeding behavior of mice lacking mPGES-1 during inflammation. Interestingly, IL-1beta failed to decrease food intake in mPGES-1(-/-) mice, although these animals developed anorexia in response to a PGE2 injection. Taken together, our results demonstrate that mPGES-1, which is strongly upregulated during inflammation in central structures involved in feeding control, is essential for immune anorexic behavior and thus may constitute a potential therapeutic target.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1531-2267
pubmed:author
pubmed:issnType
Electronic
pubmed:day
16
pubmed:volume
25
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
485-92
pubmed:meshHeading
pubmed-meshheading:16554545-Animals, pubmed-meshheading:16554545-Anorexia, pubmed-meshheading:16554545-Body Weight, pubmed-meshheading:16554545-Cyclooxygenase 2, pubmed-meshheading:16554545-Dinoprostone, pubmed-meshheading:16554545-Eating, pubmed-meshheading:16554545-Hypothalamus, pubmed-meshheading:16554545-Injections, Intraperitoneal, pubmed-meshheading:16554545-Injections, Intraventricular, pubmed-meshheading:16554545-Interleukin-1beta, pubmed-meshheading:16554545-Intramolecular Oxidoreductases, pubmed-meshheading:16554545-Male, pubmed-meshheading:16554545-Mice, pubmed-meshheading:16554545-Mice, Inbred DBA, pubmed-meshheading:16554545-Mice, Knockout, pubmed-meshheading:16554545-RNA, Messenger, pubmed-meshheading:16554545-Rats, pubmed-meshheading:16554545-Rats, Wistar, pubmed-meshheading:16554545-Time Factors, pubmed-meshheading:16554545-Up-Regulation, pubmed-meshheading:16554545-Vagus Nerve
pubmed:year
2006
pubmed:articleTitle
Involvement of central microsomal prostaglandin E synthase-1 in IL-1beta-induced anorexia.
pubmed:affiliation
Laboratoire de Physiologie Neurovégétative, UMR 6153 Centre National de la Recherche Scientifique-1147 Institut National de la Recherche Agronomique, Université Paul Cézanne, Marseille, France.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't