Effects of endotoxin on zinc metabolism in human volunteers.
Gaetke, Lisa M., Craig J. McClain, Ramesh T. Talwalkar, and Steven I.
Shedlofsky.
Departments of Nutritional Sciences and Internal Medicine,
University of Kentucky, and the Lexington Veterans Administration
Medical Center, Lexington, Kentucky 40506
APStracts 4:0032E, 1997.
After stress or trauma, the serum zinc concentration decreases. This
study evaluated possible mechanisms for hypozincemia utilizing a
human endotoxemia model. Two doses of endotoxin (LPS) were
administered on consecutive mornings to twelve healthy volunteers and
each subject was also studied after saline injection. Blood was
analyzed for zinc, cytokines (tumor necrosis factor-[alpha] and
interleukin-6), albumin, albumin-zinc binding, and C-reactive protein
(CRP). Serial 24 hour urine collections were analyzed for zinc. Each
LPS dose briefly increased plasma cytokine concentrations and
decreased the serum zinc concentration. Serum albumin, the major zinc
binding protein, did not decrease, but a progressive increase in C
-reactive protein was found. LPS did not alter zinc binding affinity
to serum albumin. Urine zinc losses were not increased. We conclude
that hypozincemia in this model cannot be explained by decreased
serum albumin, changes in serum albumin-zinc binding, or increased
urinary zinc excretion. Since hypozincemia was transient and followed
cytokine peaks, we postulate that LPS stimulated hypozincemia is
mediated, at least partly, by a cytokine-directed internal
redistribution of zinc.
Received 12 February 1996; accepted in final form 25 July 1996.
APS Manuscript Number E82-6.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1997 The American Physiological Society.
Published in APStracts on 19 February 1997