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Abstract
As compared to 7 normolipidemic donors, the maximal velocity of sodium-lithium countertransport
was accelerated by nearly 70% in 10 patients with elevated levels of triglyceride-rich
lipoproteins and tended to be stimulated also in 5 patients with hypercholesterolemia.
No significant differences were observed between normolipidemia and both hyperlipidemic
groups for the apparent affinities of the transport system for intracellular sodium
and extracellular lithium. Strong positive relations of the maximal activity of sodium-lithium
countertransport to the percentages of red cell membrane phosphatidylcholine (r = 0.85, 2P < 0.001), the phosphatidylcholine/sphingomyelin (r = 0.82, 2P < 0.001) and the phosphatidylcholine/phosphatidylethanolamine ratio (r = 0.81, 2P < 0.001) were seen in all donors. A negative correlation was found to membrane sphingomyelin
(r = −0.72, 2P < 0.001). Also plasma phosphatidylcholine and sphingomyelin exhibited positive and
negative associations, respectively, to the maximal activity of sodium-lithium countertransport
(r = 0.66, 2P < 0.01 and r = −0.78, 2P < 0.001). Among several plasma lipoprotein parameters investigated, total triglycerides
or VLDL cholesterol levels showed independent relations to both the plasma and the
membrane phosphatidylcholine/sphingomyelin ratio as well as to the maximal velocity
of sodium-lithium countertransport. The results indicate that an increase in red cell
membrane phosphatidylcholine and a concomitant fall in sphingomyelin are closely associated
with the acceleration of sodium-lithium countertransport in hyperlipidemia.
Keywords
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years of follow-up in Utah.Article info
Publication history
Accepted:
November 3,
1992
Received in revised form:
October 19,
1992
Received:
July 27,
1992
Identification
Copyright
© 1993 Published by Elsevier Inc.
