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Titolo:
Tissue-specific regulation of IGF-I and IGF-binding proteins in response to TNF alpha
Autore:
Lang, CH; Nystrom, GJ; Frost, RA;
Indirizzi:
Penn State Univ, Coll Med, Dept Cellular & Mol Physiol, Hershey, PA 17033 USA Penn State Univ Hershey PA USA 17033 & Mol Physiol, Hershey, PA 17033 USA Penn State Univ, Coll Med, Dept Surg, Hershey, PA 17033 USA Penn State Univ Hershey PA USA 17033 ed, Dept Surg, Hershey, PA 17033 USA
Titolo Testata:
GROWTH HORMONE & IGF RESEARCH
fascicolo: 4, volume: 11, anno: 2001,
pagine: 250 - 260
SICI:
1096-6374(200108)11:4<250:TROIAI>2.0.ZU;2-I
Fonte:
ISI
Lingua:
ENG
Soggetto:
ACID-LABILE SUBUNIT; NECROSIS-FACTOR-ALPHA; MESSENGER-RIBONUCLEIC-ACID; GROWTH-FACTOR SYSTEM; PROMOTER ACTIVITY; SKELETAL-MUSCLE; HUMAN SERUM; RNA LEVELS; RAT-LIVER; HORMONE;
Keywords:
free IGF-I; IGF-II; IGFBP-1; IGFBP-3; ALS; mac25;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
52
Recensione:
Indirizzi per estratti:
Indirizzo: Lang, CH Penn State Univ, Coll Med, Dept Cellular & Mol Physiol, H166, Hershey, PA 17033 USA Penn State Univ H166 Hershey PA USA 17033 , Hershey, PA 17033 USA
Citazione:
C.H. Lang et al., "Tissue-specific regulation of IGF-I and IGF-binding proteins in response to TNF alpha", GROWTH H I, 11(4), 2001, pp. 250-260

Abstract

The circulating concentration of insulin-like growth factor-I (IGF-I) is regulated by both its rate of synthesis and its ability to form stable complexes with IGF-binding proteins (IGFBPs). An equilibrium between IGF-I and IGFBPs is thought to help maintain muscle protein balance. In contrast, catabolic conditions disrupt the IGF system and result in the loss of skeletal muscle protein. We have examined the mechanisms by which tumour necrosis factor alpha (TNF alpha), a catabolic cytokine, alters the IGF system. Conscious rats were infused intravenously with recombinant human TNF alpha or vehicle for 24 h. TNF alpha decreased the concentration of both total and freeIGF-I in the plasma (30-40%). This change was associated with a reduction in IGF-I mRNA expression in liver (39%), gastrocnemius (73%), soleus (46%) and heart (63%), but a 2.5-fold increase in the whole kidney. In contrast, TNF alpha did not alter IGF-II mRNA expression in skeletal muscle. TNFa also increased IGFBP-1 in the blood (4-fold) and this response was associated with an increase in IGFBP-1 mRNA expression in both liver (3-fold) and kidney (9-fold). In contrast, IGFBP-3 levels in the blood were reduced 38% in response to the infusion of TNFa. This change was accompanied by a 60-80% reduction of IGFBP-3 mRNA in liver and kidney but no significant change in muscle. Hepatic mRNA levels of the acid-labile subunit were also reduced by TNF alpha (46%). Finally, tissue expression of mac25 (also referred to IGFBP-related protein-1) mRNA was increased in gastrocnemius (50%) but remained unchanged in liver and kidney. These results more fully characterize the changes in various elements of the IGF system and, thereby, provide potentialmechanisms for the alterations in the circulating IGF system as well as for changes in tissue metabolism observed during catabolic insults associatedwith increased TNF alpha expression. (C) 2001 Harcourt Publishers Ltd.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 08/04/20 alle ore 09:02:07