g(m3)-ganglioside and Potassium-Deficiency

g(m3)-ganglioside has been researched along with Potassium-Deficiency* in 1 studies

Other Studies

1 other study(ies) available for g(m3)-ganglioside and Potassium-Deficiency

Article	Year
Glycosphingolipids modulate renal phosphate transport in potassium deficiency. Kidney international, 2001, Volume: 60, Issue:2 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 in the rat.. 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.. 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. 1184 +/- 99 pmol/5 sec/mg BBM protein in K deficiency, P < 0.02). Surprisingly, the decrease in Na/Pi cotransport activity 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 in Na/Pi transport was associated with significant alterations in BBM lipid composition, including increases in sphingomyelin, glucosylceramide, and ganglioside GM3 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-deficient rats was the same as in control rats (1148 +/- 52 in control + PDMP vs. 1152 +/- 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.. 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. Topics: Animals; Carrier Proteins; G(M3) Ganglioside; Gene Expression; Glucosylceramides; Hypokalemia; Kidney Tubules, Proximal; Kinetics; Male; Membrane Fluidity; Microvilli; Oocytes; Phosphates; Phosphorus; Potassium Deficiency; Rats; Rats, Sprague-Dawley; Receptors, Virus; RNA, Messenger; Sodium-Phosphate Cotransporter Proteins; Sodium-Phosphate Cotransporter Proteins, Type I; Sodium-Phosphate Cotransporter Proteins, Type II; Sodium-Phosphate Cotransporter Proteins, Type III; Symporters; Xenopus laevis	2001

Article

Year

Glycosphingolipids modulate renal phosphate transport in potassium deficiency.

Kidney international, 2001, Volume: 60, Issue:2

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 in the rat.. 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.. 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. 1184 +/- 99 pmol/5 sec/mg BBM protein in K deficiency, P < 0.02). Surprisingly, the decrease in Na/Pi cotransport activity 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 in Na/Pi transport was associated with significant alterations in BBM lipid composition, including increases in sphingomyelin, glucosylceramide, and ganglioside GM3 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-deficient rats was the same as in control rats (1148 +/- 52 in control + PDMP vs. 1152 +/- 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.. 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.

Topics: Animals; Carrier Proteins; G(M3) Ganglioside; Gene Expression; Glucosylceramides; Hypokalemia; Kidney Tubules, Proximal; Kinetics; Male; Membrane Fluidity; Microvilli; Oocytes; Phosphates; Phosphorus; Potassium Deficiency; Rats; Rats, Sprague-Dawley; Receptors, Virus; RNA, Messenger; Sodium-Phosphate Cotransporter Proteins; Sodium-Phosphate Cotransporter Proteins, Type I; Sodium-Phosphate Cotransporter Proteins, Type II; Sodium-Phosphate Cotransporter Proteins, Type III; Symporters; Xenopus laevis

2001