rdf:type |
|
lifeskim:mentions |
umls-concept:C0010453,
umls-concept:C0023796,
umls-concept:C0033554,
umls-concept:C0079189,
umls-concept:C0085862,
umls-concept:C0206131,
umls-concept:C0441712,
umls-concept:C0547047,
umls-concept:C1149837,
umls-concept:C1299583,
umls-concept:C1549571,
umls-concept:C1608386
|
pubmed:issue |
1
|
pubmed:dateCreated |
1992-8-14
|
pubmed:abstractText |
We previously showed that indomethacin blocked the effect of tumor necrosis factor (TNF) and other cytokines on lipolysis. We now show that TNF stimulates prostaglandin (PG) production, enhances lipolysis and decreases lipoprotein lipase (LPL) activity in 3T3-F442A adipocytes and indomethacin blocks these activities, suggesting that the actions of TNF are mediated by PG's. However, exogenous PGE2 at the levels induced by TNF is not sufficient to affect lipolysis or LPL activity and low doses of indomethacin and flurbiprofen block PG production without affecting TNF's action. Interleukin-1 and interferon-alpha and gamma induce lipolysis and decrease LPL activity but do not stimulate much PG production. These results demonstrate that cytokines enhance lipolysis and decrease LPL activity in 3T3 adipocytes by a PG independent mechanism.
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pubmed:grant |
|
pubmed:language |
eng
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pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Cytokines,
http://linkedlifedata.com/resource/pubmed/chemical/Dinoprostone,
http://linkedlifedata.com/resource/pubmed/chemical/Flurbiprofen,
http://linkedlifedata.com/resource/pubmed/chemical/Indomethacin,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon Type I,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Lipoprotein Lipase,
http://linkedlifedata.com/resource/pubmed/chemical/Prostaglandins,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
|
pubmed:issn |
0006-291X
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pubmed:author |
|
pubmed:issnType |
Print
|
pubmed:day |
15
|
pubmed:volume |
186
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
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pubmed:pagination |
237-43
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:1632769-3T3 Cells,
pubmed-meshheading:1632769-Adipose Tissue,
pubmed-meshheading:1632769-Animals,
pubmed-meshheading:1632769-Cells, Cultured,
pubmed-meshheading:1632769-Cytokines,
pubmed-meshheading:1632769-Dinoprostone,
pubmed-meshheading:1632769-Flurbiprofen,
pubmed-meshheading:1632769-Humans,
pubmed-meshheading:1632769-Indomethacin,
pubmed-meshheading:1632769-Interferon Type I,
pubmed-meshheading:1632769-Interferon-gamma,
pubmed-meshheading:1632769-Interleukin-1,
pubmed-meshheading:1632769-Kinetics,
pubmed-meshheading:1632769-Lipolysis,
pubmed-meshheading:1632769-Lipoprotein Lipase,
pubmed-meshheading:1632769-Mice,
pubmed-meshheading:1632769-Prostaglandins,
pubmed-meshheading:1632769-Recombinant Proteins,
pubmed-meshheading:1632769-Tumor Necrosis Factor-alpha
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pubmed:year |
1992
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pubmed:articleTitle |
Cytokines stimulate lipolysis and decrease lipoprotein lipase activity in cultured fat cells by a prostaglandin independent mechanism.
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pubmed:affiliation |
Department of Medicine, University of California, San Francisco.
|
pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, U.S. Gov't, Non-P.H.S.
|