AJCN Tufts Nutrition Symposium, Boston & Online Sept 2009
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American Journal of Clinical Nutrition, Vol. 82, No. 6, 1357, December 2005
© 2005 American Society for Clinical Nutrition

LETTER TO THE EDITOR

Use of mathematical modeling to study copper metabolism in humans

Walter S Watson

Southern General Hospital
Nuclear Medicine Department
Govan Road
Glasgow G51 4TF
United Kingdom
E-mail: wswatson{at}f2s.com

Thomas DB Lyon

Department of Clinical Biochemistry
Royal Infirmary
Glasgow
United Kingdom

Dear Sir:

In a recent article in the Journal, Harvey et al (1) described a mathematical model used to study copper metabolism in humans. The model involved the subdivision of body copper into compartments that ideally have some physiologic relevance. The amount of copper in each of the compartments and the flow rates of copper between the compartments could be quantified with the use of tracer data as input in the model.

One of the results of the model was that the half-life of ceruloplasmin was {approx}27 d, which the authors suggested compared well with the value of 20 d that was previously reported by one of us (TDBL) (2). In that 1995 article, the "biological half-time of copper in plasma ... was found to be 19.5 ± 5 days (mean ± SD)". However, as stated in that article, this was not the half-life of ceruloplasmin. Although ceruloplasmin-bound copper accounts for >90% of plasma copper, the biological half-life of copper in plasma after ingestion of a copper tracer is not the half-life of ceruloplasmin, because the half-life of copper is influenced not only by the exit from the ceruloplasmin compartment but also by the input of recycled copper into the compartment from other longer-lived compartments. Evidence for this is included in that 1995 article, ie, the biological half-life for clearance of the tracer from the plasma pool was increased to a median half-life of 43 d in Wilsons disease heterozygotes, in whom, as previously described (3), decreased biliary excretion of copper results in a greater whole-body half-life than in control subjects.

Harvey et al (1) also state that "Only one compartmental model of copper metabolism has been developed for humans"—that of Scott and Turnlund (4). However, many articles published since the 1960s have described compartmental models for human copper metabolism (5–9).

ACKNOWLEDGMENTS

The authors had no conflicts of interest.

REFERENCES

  1. Harvey LJ, Dainty JR, Hollands WJ, et al. Use of mathematical modeling to study copper metabolism in humans. Am J Clin Nutr 2005;81:807–13.[Abstract/Free Full Text]
  2. Lyon TD, Fell GS, Gaffney D, et al. Use of a stable copper isotope (65Cu) in the differential diagnosis of Wilson's disease. Clin Sci (Lond) 1995;88:727–32.[Medline]
  3. O'Reilly S, Strickland GT Jr, Weber PM, Beckner WM, Shipley L. Abnormalities of the physiology of copper in Wilson's disease. I. The whole-body turnover of copper. Arch Neurol 1971;24:385–90.
  4. Scott CS, Turnlund JR. Compartmental model of copper metabolism in adult men. J Nutr Biochem 1994;5:342–50.
  5. Cartwright GE, Wintrobe MM. Copper metabolism in normal subjects. Am J Clin Nutr 1964;14:224–32.[Abstract/Free Full Text]
  6. Chervu LR, Sternlieb I. Dosimetry of copper radionuclides. J Nucl Med 1974;15:1011–3.[Abstract/Free Full Text]
  7. Bernard SR. Metabolic model and dosimetric data for copper. Bull Math Biol 1978;40:265–9.[Medline]
  8. Blincoe C. Computer simulation of normal and pathological copper metabolism in man. Comput Biol Med 1993;23:49–55.[Medline]
  9. Buckley WT. Application of compartmental modeling to determination of trace element requirements in humans. J Nutr 1996;126:2312S–9S.




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