Erythrocyte Sodium-Lithium Countertransport Activity in Non-Nephropathic Diabetic Twins

Abstract

An elevation in Na-Li countertransport activity has been noted in non-nephropathic normotensive twin pairs both discordant and concordant for IDDM. The potential genetic contribution to the altered behavior of the countertransporter was similar in both types of twins studied, and individual Na-Li countertransport activities were not significantly related to either duration of diabetes or metabolic control.

Sodium–lithium countertransport is increased in normoalbuminuric type 1 diabetes but is not related to other risk factors for microangiopathy

“…Na / Li CT activity may rather be a sensitive marker of changes in the composition of the cell membrane or alterations in intracellular ion-exchangers or signalling systems, which may predispose to cell injury. Such alterations may be the result of environmentally [14,[34][35][36] or genetically determined factors [13,37].…”

Kinetic characteristics of the erythrocyte sodium-lithium countertransporter in black normotensive subjects compared with three other ethnic groups

“…Weak correlations were observed between countertransport activity and several cardiovascular risk factors; all these correlations have been noted previously. 19,22 It is likely that the failure to detect similar patterns of correlation between these risk factors and countertransport activity across the four study groups was due both to the nature of the correlations, which tend on the whole to be weak, and to the relatively small group sizes. It seems unlikely that any of the clinical differences that were noted between the groups, such as the increased height and weight or reduced plasma triglyceride concentrations in the black subjects, were directly related to the observed differences in countertransport activity.…”

“…36,37 The observed difference in the behaviour of the sodium-lithium countertransporter in a single ethnic group suggests that this phenomenon may be genetically determined. SLC activity has long been known to be under genetic influence, 9,19,20,26 while both V max and k Na have shown familial associations. 39,40 The present study was not designed to explore the question of whether there are direct genetic influences on expression of the countertransporter protein or whether the altered behaviour of the countertransporter occurs secondarily to some other genetically determined metabolic alteration.…”

“…This finding is in agreement with earlier work which showed expression of countertransport activity to be dependent on plasma lipid status, and in particular with plasma triglyceride concentration. 19,22 More recent work has demonstrated that it is the V max of the countertransporter which is sensitive to plasma lipid status; with emphasis on HDL cholesterol and plasma triglyceride concentrations. 29 Despite the present study finding no correlation between triglyceride concentration and V max values in the black group, the lower triglyceride concentration in these subjects, noted on several occasions previously, [30][31][32] may still be relevant.…”

“…Determination of SLC activity and kinetics SLC activity was determined using an established method, which has been described previously in detail, 19 and was based on choline serving as the sodium-free medium. 20 Erythrocytes were loaded by incubation for 3 h in lithium-rich loading solution, following which, aliquots of packed cells were added to either choline or sodium-based medium (149 mmol/l) plus (mmol/l): MgCl 2 , 1; glucose, 10; ouabain, 0.1; Tris-MOPS, pH 7.4 at 37°C.…”