Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3 Pt 1
pubmed:dateCreated
1996-7-5
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.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0002-9513
pubmed:author
pubmed:issnType
Print
pubmed:volume
270
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
E430-7
pubmed:dateRevised
2007-11-14
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
pubmed:year
1996
pubmed:articleTitle
IL-1 receptor antagonist attenuates sepsis-induced alterations in the IGF system and protein synthesis.
pubmed:affiliation
Department of Surgery, State University of New York at Stony Brook, New York 11794-8191, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't