Source:http://linkedlifedata.com/resource/pubmed/id/17464341
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
2007-4-27
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pubmed:abstractText |
Acylation-stimulating protein (ASP) and interaction with its receptor C5L2 influences adipocyte metabolism. We examined insulin resistance and differentiation-mediated regulation of C5L2 and the mechanistic impact on both C5L2 cell-surface protein and ligand binding to the receptor. C5L2 mRNA increased 8.7-fold with differentiation in 3T3-L1 cells (p < 0.0001) by day 9. In preadipocytes, insulin and dexamethasone increased C5L2 mRNA (1 micromol/L insulin resulted in a 2.6-fold increase, p < 0.01; 10 nmol/L dexamethasone resulted in a 17.9-fold increase, p < 0.01) and C5L2 cell-surface protein (100 nmol insulin resulted in a 2.7-fold increase, p < 0.001; 10 nmol/L dexamethasone resulted in a 2.8-fold increase, p < 0.001). In adipocytes, 100 nmol/L insulin increased C5L2 mRNA and ASP binding (respectively, 1.3-fold, p < 0.01; and 2.4-fold, p < 0.05). Dexamethasone decreased ligand binding (-60%, p < 0.02) without changing mRNA. Tumor necrosis factor alpha decreased C5L2 mRNA (-88% in preadipocytes and -38% in adipocytes, p < 0.001), C5L2 cell-surface protein (-53% in preadipocytes, p < 0.0001), and ASP binding (-60% and -49% in, respectively, preadipocytes and adipocytes, p < 0.05). Conversely, 1 micromol/L and 10 nmol/L rosiglitazone increased, respectively, C5L2 mRNA (9.3-fold, p < 0.0001) and ASP binding (2.4-fold, p < 0.05). Thus, C5L2 mRNA increases with differentiation, insulin, and thiazolidinedione treatment, and decreases with tumor necrosis factor alpha, all of which results in functional changes in ASP-C5L2 response and may have implications for human metabolism.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/2,4-thiazolidinedione,
http://linkedlifedata.com/resource/pubmed/chemical/Complement C3a,
http://linkedlifedata.com/resource/pubmed/chemical/Dexamethasone,
http://linkedlifedata.com/resource/pubmed/chemical/Glucocorticoids,
http://linkedlifedata.com/resource/pubmed/chemical/Gpr77 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Hypoglycemic Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Chemokine,
http://linkedlifedata.com/resource/pubmed/chemical/Thiazolidinediones,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha,
http://linkedlifedata.com/resource/pubmed/chemical/complement C3a, des-Arg-(77)
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0829-8211
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
85
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
11-21
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pubmed:dateRevised |
2008-4-5
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pubmed:meshHeading |
pubmed-meshheading:17464341-Acylation,
pubmed-meshheading:17464341-Adipocytes,
pubmed-meshheading:17464341-Animals,
pubmed-meshheading:17464341-Cell Differentiation,
pubmed-meshheading:17464341-Cell Line,
pubmed-meshheading:17464341-Complement C3a,
pubmed-meshheading:17464341-Dexamethasone,
pubmed-meshheading:17464341-Glucocorticoids,
pubmed-meshheading:17464341-Hypoglycemic Agents,
pubmed-meshheading:17464341-Insulin Resistance,
pubmed-meshheading:17464341-Mice,
pubmed-meshheading:17464341-Receptors, Chemokine,
pubmed-meshheading:17464341-Thiazolidinediones,
pubmed-meshheading:17464341-Tumor Necrosis Factor-alpha
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pubmed:year |
2007
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pubmed:articleTitle |
The ASP receptor C5L2 is regulated by metabolic hormones associated with insulin resistance.
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pubmed:affiliation |
Medicine, McGill University Health Center, Montreal, Canada.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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