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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3 Pt 1
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pubmed:dateCreated |
1996-7-5
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pubmed:abstractText |
The purpose of the present investigation was to determine whether endogenously produced interleukin (IL)-1 mediates the changes in insulin-like growth factor (IGF) I and IGF binding proteins (IGFBP) induced by chronic abdominal sepsis in rats and to correlate the changes in the IGF system with the alternations in protein synthesis. A constant infusion of IL-1 receptor antagonist (IL-1ra) was begun after the induction of sepsis and was continued for 5 days. Sepsis decreased IGF-I levels in the blood, liver, and gastrocnemius muscle, increased the content in the kidney, and did not alter IGF-I levels in heart, jejunum, and spleen. IL-1ra attenuated the sepsis-induced decrease in plasma IGF-I and completely prevented the changes in IGF-I observed in liver, kidney, and the gastrocnemius. IGFBP-1 was increased in the blood, liver, and muscle of septic rats. IL-1ra prevented this increase in IGFBP-1 in blood and liver but not in muscle. The rate of in vivo protein synthesis was decreased in the gastrocnemius and kidney and unaltered in the heart, liver, jejunum, and spleen. A strong linear correlation existed between levels of IGF-I and the rate of protein synthesis determined simultaneously in the gastrocnemius. These results provide evidence for the role of IL-1 as an endogenous mediator of the sepsis-induced changes in IGF-I and IGFBP-1 and suggest that the accompanying changes in muscle protein synthesis are partially mediated via changes in IGF-I.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Corticosterone,
http://linkedlifedata.com/resource/pubmed/chemical/Growth Hormone,
http://linkedlifedata.com/resource/pubmed/chemical/Insulin-Like Growth Factor Binding...,
http://linkedlifedata.com/resource/pubmed/chemical/Insulin-Like Growth Factor I,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin 1 Receptor Antagonist...,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Sialoglycoproteins
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
0002-9513
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
270
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
E430-7
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:8638689-Animals,
pubmed-meshheading:8638689-Bacteremia,
pubmed-meshheading:8638689-Bacteroides Infections,
pubmed-meshheading:8638689-Corticosterone,
pubmed-meshheading:8638689-Escherichia coli Infections,
pubmed-meshheading:8638689-Growth Hormone,
pubmed-meshheading:8638689-Insulin-Like Growth Factor Binding Protein 1,
pubmed-meshheading:8638689-Insulin-Like Growth Factor I,
pubmed-meshheading:8638689-Interleukin 1 Receptor Antagonist Protein,
pubmed-meshheading:8638689-Interleukin-1,
pubmed-meshheading:8638689-Jejunum,
pubmed-meshheading:8638689-Kidney,
pubmed-meshheading:8638689-Liver,
pubmed-meshheading:8638689-Male,
pubmed-meshheading:8638689-Muscle, Skeletal,
pubmed-meshheading:8638689-Myocardium,
pubmed-meshheading:8638689-Organ Specificity,
pubmed-meshheading:8638689-Rats,
pubmed-meshheading:8638689-Rats, Sprague-Dawley,
pubmed-meshheading:8638689-Reference Values,
pubmed-meshheading:8638689-Sialoglycoproteins,
pubmed-meshheading:8638689-Spleen
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pubmed:year |
1996
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pubmed:articleTitle |
IL-1 receptor antagonist attenuates sepsis-induced alterations in the IGF system and protein synthesis.
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pubmed:affiliation |
Department of Surgery, State University of New York at Stony Brook, New York 11794-8191, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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