As. Wierzbicki et al., Relation between sodium-lithium countertransport and hypertriglyceridemia in type V hyperlipidemia, AM J HYPERT, 14(1), 2001, pp. 32-37
Sodium-lithium countertransport (SLC) kinetics were measured in 30 patients
with type V hyperlipidemia, 30 patients with type IIB hyperlipidemia on si
milar treatment, and 30 age- and sex-matched healthy controls. Clinical and
laboratory data including basic anthropometry and blood pressure were obta
ined and blood was taken for detailed lipid biochemistry, glucose, insulin,
and leptin measurements. Patients with type V hyperlipidemia were normoten
sive but more obese than controls, had elevated triglycerides, very low-den
sity lipoprotein, glucose, and insulin: and reduced HDL cholesterol compare
d with type IIb controls. The median SLC activity (0.23 v 0.21 mmol Li+/L R
BC/h) and median maximal velocity (0.33 v 0.31 mmol Li+/L RBC/h) were incre
ased, but not significantly, compared to controls. In patients with type V
hyperlipidemia SLC maximal velocity correlated with log triglycerides (r(2)
= 0.853; P < .001) and log very low-density lipoprotein (VLDL) triglycerid
es (r(2) = 0.947; P < .001). Sodium-lithium countertransport maximal veloci
ty correlated weakly with the homeostasis model assessment index of insulin
resistance (r(2) = 0.2241 P = .06). The sodium affinity of the transporter
did not differ between the groups and was independent of any of clinical o
r biochemical parameter studied. We conclude that VLDL triglyceride is stro
ngly correlated with SLC maximal velocity and activity in patients with typ
e V hyperlipidemia. (C) 2001 American Journal of Hypertension, Ltd.