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Titolo:
THE IGF-I AXIS IN KIDNEY AND SKELETAL-MUSCLE OF POTASSIUM DEFICIENT RATS
Autore:
HSU FW; TSAO T; RABKIN R;
Indirizzi:
VET AFFAIRS MED CTR,DEPT MED,3801 MIRANDA AVE PALO ALTO CA 94304 VET AFFAIRS MED CTR,DEPT MED PALO ALTO CA 94304 STANFORD UNIV,DEPT MED PALO ALTO CA 94304
Titolo Testata:
Kidney international
fascicolo: 2, volume: 52, anno: 1997,
pagine: 363 - 370
SICI:
0085-2538(1997)52:2<363:TIAIKA>2.0.ZU;2-C
Fonte:
ISI
Lingua:
ENG
Soggetto:
GROWTH-FACTOR-I; PROTEIN-RESTRICTED RATS; K+ PUMP CONCENTRATION; GH-BINDING-PROTEIN; DEPLETED RATS; RENAL GROWTH; HORMONE; RECEPTOR; FAILURE; HYPERTROPHY;
Keywords:
POTASSIUM DEFICIENCY; RENAL HYPERTROPHY; GROWTH RETARDATION; INSULIN-LIKE GROWTH FACTOR I; TUBULOINTERSTITIAL FIBROSIS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
32
Recensione:
Indirizzi per estratti:
Citazione:
F.W. Hsu et al., "THE IGF-I AXIS IN KIDNEY AND SKELETAL-MUSCLE OF POTASSIUM DEFICIENT RATS", Kidney international, 52(2), 1997, pp. 363-370

Abstract

Potassium deficiency in the rat results in growth retardation, musclewasting and renal hypertrophy. This study tests the thesis that K deficiency leads to tissue distinct changes in the local IGF-I system andcell sensitivity to IGF-I that favors renal enlargement on the one hand and impaired muscle growth on the other. In rats after eight days of K deficiency, compared to pair-fed control rats, food utilization and muscle and body wt gain were attenuated while the kidneys enlarged. In muscle GH receptor and IGF-I gene expression, IGF-I peptide and IGFbinding protein-5 (IGBFBP) levels were decreased. Together with reduced food utilization, these changes may contribute to the attenuated muscle growth. In the enlarged kidneys despite a fall in IGF-I mRNA level. IGF-I peptide concentration was increased more than twofold. This increase in IGF-I could be caused by the increase in kidney IGFBP-1 gene and protein expression and the decrease in kidney IGF-I degrading activity noted in K deficiency. Treatment with IGF-I failed to induce body or muscle growth, but induced a further increase in kidney size andenlargement of the spleen. Thus, in K deficiency the spontaneous increase in IGF-I levels in the kidney that is IGF-I sensitive may well bea cause of the renal hypertrophy.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/07/20 alle ore 18:30:01