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Titolo:
Glycosphingolipids modulate renal phosphate transport in potassium deficiency
Autore:
Zajicek, HK; Wang, HM; Puttaparthi, K; Halaihel, N; Markovich, D; Shayman, J; Beliveau, R; Wilson, P; Rogers, T; Levi, M;
Indirizzi:
Vet Adm Med Ctr, Dallas, TX 75216 USA Vet Adm Med Ctr Dallas TX USA 75216Vet Adm Med Ctr, Dallas, TX 75216 USA Univ Texas, SW Med Ctr, Dept Internal Med, Dallas, TX USA Univ Texas Dallas TX USA , SW Med Ctr, Dept Internal Med, Dallas, TX USA Univ Queensland, Dept Physiol & Pharmacol, Brisbane, Qld, Australia Univ Queensland Brisbane Qld Australia armacol, Brisbane, Qld, Australia Univ Michigan, Ctr Med, Dept Internal Med, Ann Arbor, MI 48109 USA Univ Michigan Ann Arbor MI USA 48109 nternal Med, Ann Arbor, MI 48109 USA Univ Quebec, Oncol Mol Lab, Montreal, PQ H3C 3P8, Canada Univ Quebec Montreal PQ Canada H3C 3P8 Lab, Montreal, PQ H3C 3P8, Canada
Titolo Testata:
KIDNEY INTERNATIONAL
fascicolo: 2, volume: 60, anno: 2001,
pagine: 694 - 704
SICI:
0085-2538(200108)60:2<694:GMRPTI>2.0.ZU;2-V
Fonte:
ISI
Lingua:
ENG
Soggetto:
BRUSH-BORDER MEMBRANES; GENERALIZED POLARIZATION; LAURDAN FLUORESCENCE; LIPID-COMPOSITION; I COTRANSPORTER; DOWN-REGULATION; MESSENGER-RNA; PI TRANSPORT; RAT-KIDNEY; DEPLETION;
Keywords:
Na/Pi cotransport proteins; lipid fluidity; membrane lipid dynamics; hypokalemia; glucosylceramide; ganglioside GM(3); brush-border membrane; proximal tubule;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
74
Recensione:
Indirizzi per estratti:
Indirizzo: Levi, M Vet Adm Med Ctr, 4500 S Lancaster Rd,MC 151, Dallas, TX 75216 USA Vet Adm Med Ctr 4500 S Lancaster Rd,MC 151 Dallas TX USA 75216 USA
Citazione:
H.K. Zajicek et al., "Glycosphingolipids modulate renal phosphate transport in potassium deficiency", KIDNEY INT, 60(2), 2001, pp. 694-704

Abstract

Background. Potassium (K) deficiency (KD) and/or hypokalemia have been associated with disturbances of phosphate metabolism The purpose of the present study was to determine the cellular mechanisms that mediate the impairment of renal proximal tubular Na/Pi cotransport in a model of K deficiency inthe rat. Methods. K deficiency in the rat was achieved by feeding rats a K-deficient diet for seven days. which resulted in a marked decrease in serum and tissue K content. Results. K deficiency resulted in a marked increase in urinary Pi excretion and a decrease in the V-max of brush-border membrane (BBM) Na/Pi cotransport activity (1943 95 in control vs. 1183 +/- 99 pmol/5 sec/mg BBM protein in K deficiency. P < 0.02). Surprisingly. the decrease in Na/Pi cotransportactivity was associated with increases in the abundance of type I (NaPi-1). and type II (NaPi-2) and type III (Glvr-1) Na/Pi protein. The decrease inNa/Pi transport was associated with significant alterations in BBM lipid composition, including increases in sphingomyelin. glucosylceramide. and ganglioside GM, content and a decrease in BBM lipid fluidity. Inhibition of glucosylceramide synthesis resulted in increases in BBM Na/Pi cotransport activity in control and K-deficient rats. The resultant Na/Pi cotransport activity in K-deficit nt rats was the same as in control rats (1148 +/- 52 in control + PDMP vs. 11.52 +/- 61 pmol/5 sec/mg BBM protein in K deficiency + PDMP). These changes in transport activity occurred independent of further changes in BBM NaPi-2 protein or renal cortical NaPi-2 mRNA abundance. Conclusion. K deficiency in the rat causes inhibition of renal Na/Pi cotransport activity by post-translational mechanisms that are mediated in part through alterations in glucosylceramide content and membrane lipid dynamics.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/10/20 alle ore 21:41:19