Source:http://linkedlifedata.com/resource/pubmed/id/20961858
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
2011-1-3
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pubmed:abstractText |
Obesity is associated with a variety of disorders and is a significant health problem in developed countries. One factor controlling the level of adiposity is the differentiation of cells into adipocytes. Adipocyte differentiation requires expression of peroxisome proliferator-activated receptor ? (PPAR?), which is activated by ligands to regulate expression of genes involved in adipocyte differentiation. Although 15-deoxy-?(12,14)-prostaglandin (PG) J(2) (15d-PGJ(2)) has long been known to be a potent activator of PPAR?, the importance of its synthesis in adipose tissue in vivo is not clear. The current study utilized mice deficient in cyclooxygenase-2 (COX-2) to examine the role of COX-2-derived PGs as in vivo modulators of adiposity. As compared with strain- and age-matched wild-type controls, the genetic deficiency of COX-2 resulted in a significant reduction in total body weight and percent body fat. Although there were no significant differences in food consumption between groups, COX-2-deficient mice showed increased metabolic activity. Epididymal adipose tissue from wild-type mice produced a significantly greater level of 15d-PGJ(2), as compared with adipose tissue isolated from mice deficient in COX-2. Furthermore, production of the precursor required for 15d-PGJ(2) formation, PGD(2), was also significantly reduced in COX-2-deficient adipose tissue. The expression of markers for differentiated adipocytes was significantly reduced in adipose tissue from COX-2-deficient mice, whereas preadipocyte marker expression was increased. Macrophage-dependent inflammation was also significantly reduced in adipose tissue of COX-2-deficient mice. These findings suggest that reduced adiposity in COX-2-deficient mice results from attenuated PPAR? ligand production and adipocyte differentiation.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
1083-351X
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:day |
7
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pubmed:volume |
286
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
889-98
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pubmed:meshHeading |
pubmed-meshheading:20961858-Adipocytes, White,
pubmed-meshheading:20961858-Adipose Tissue,
pubmed-meshheading:20961858-Aging,
pubmed-meshheading:20961858-Animals,
pubmed-meshheading:20961858-Biological Markers,
pubmed-meshheading:20961858-Cell Differentiation,
pubmed-meshheading:20961858-Cyclooxygenase 2,
pubmed-meshheading:20961858-Inflammation,
pubmed-meshheading:20961858-Male,
pubmed-meshheading:20961858-Mice,
pubmed-meshheading:20961858-Prostaglandins
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pubmed:year |
2011
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pubmed:articleTitle |
Cyclooxygenase-2 deficiency attenuates adipose tissue differentiation and inflammation in mice.
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pubmed:affiliation |
Department of Pharmaceutical Sciences, College of Pharmacy, University of Kentucky, Lexington, Kentucky 40536, USA.
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pubmed:publicationType |
Journal Article
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