Controversies surrounding erythrocyte sodium-lithium countertransport

Effects of lipids in patients with familial hypercholesterolaemia on the kinetics of the sodium-lithium countertransporter

“…[1][2][3][4][5][6][7][8][9] However, our data do not show any relationship of SLC kinetic parameters with markers of insulin resistance. This relationship has been described as being absent in other normotensive populations.…”

“…1-9,13,14 Though many studies have been conducted on this transporter its exact mechanism remains obscure. 1 Some studies have suggested that SLC V max is altered by membrane triacylglycerols resulting in alterations of phospholipid profile and exposure of sulph-hydryl groups 9,15,16 yet in polygenic mixed hyperlipidaemic patients it has always been thought that the mechanism might involve insulin sensitivity rather than be related to triglyceride concentration. It has also been shown that SLC activity can be affected by the identity of fatty acids with a reduction in activity with the alpha-methylated fatty acids in Refsum's disease.…”

“…1 Associations have been demonstrated with non-insulin dependent diabetes mellitus, 2 essential hypertension, [3][4][5] and risk of coronary artery disease. [6][7][8] The activity of SLC can be resolved into kinetic components of maximal turnover velocity (V max ) and substrate affinity (K m ).…”

“…[6][7][8] The activity of SLC can be resolved into kinetic components of maximal turnover velocity (V max ) and substrate affinity (K m ). 1,2,9 Few studies have examined the inter-relationship of SLC kinetics and primary dyslipidaemia. Membrane cholesterol is known to influence transport processes 10 so in this study investigated the effects of severe hypercholesterolaemia in patients with heterozygous familial hypercholesterolaemia (FH) on SLC activity and kinetics.…”

Urinary retinol-binding protein (RBP) excretion and erythrocyte sodium-lithium countertransport (SLC) activity in a cohort of healthy normotensive subjects

“…1,2 In healthy subjects, an inverse relationship has been noted between sodium-lithium countertransport (SLC) activity and fractional excretion of lithium; an index of renal proximal tubular function. 3 Correlations have been noted in several studies between SLC activity and the plasma concentrations of urea and creatinine, which can be dependent on renal clearance, 2,4,5 and glomerular hyperfiltration in hypertensive patients.…”