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Research Article Free access | 10.1172/JCI105975

Dietary perturbation of calcium metabolism in normal man: compartmental analysis

James M. Phang, Mones Berman, Gerald A. Finerman, Robert M. Neer, Leon E. Rosenberg, and Theodore J. Hahn

1Metabolism Branch, National Cancer Institute, and the Mathematical Research Branch, National Institute of Arthritis and Metabolic Diseases, National Institutes of Health, Bethesda, Maryland 20014

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1Metabolism Branch, National Cancer Institute, and the Mathematical Research Branch, National Institute of Arthritis and Metabolic Diseases, National Institutes of Health, Bethesda, Maryland 20014

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1Metabolism Branch, National Cancer Institute, and the Mathematical Research Branch, National Institute of Arthritis and Metabolic Diseases, National Institutes of Health, Bethesda, Maryland 20014

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1Metabolism Branch, National Cancer Institute, and the Mathematical Research Branch, National Institute of Arthritis and Metabolic Diseases, National Institutes of Health, Bethesda, Maryland 20014

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1Metabolism Branch, National Cancer Institute, and the Mathematical Research Branch, National Institute of Arthritis and Metabolic Diseases, National Institutes of Health, Bethesda, Maryland 20014

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1Metabolism Branch, National Cancer Institute, and the Mathematical Research Branch, National Institute of Arthritis and Metabolic Diseases, National Institutes of Health, Bethesda, Maryland 20014

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Published January 1, 1969 - More info

Published in Volume 48, Issue 1 on January 1, 1969
J Clin Invest. 1969;48(1):67–77. https://doi.org/10.1172/JCI105975.
© 1969 The American Society for Clinical Investigation
Published January 1, 1969 - Version history
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Abstract

The effect of dietary calcium intake on calcium metabolism was studied in eight normal volunteers by multicompartmental analysis of radiocalcium and balance data. In paired studies of six normal subjects on normal and high or low calcium intakes, necessary and sufficient criteria were used to determine changes in calcium metabolic parameters produced by alterations in dietary calcium. These changes involved gastrointestinal calcium absorption rate, renal and endogenous fecal rate constants, and bone resorption rate. Bone accretion rate and compartment sizes need not change between the paired studies. The changes of parameters involving kidney, gut, and bone were in a direction to support calcium homeostasis and were compatible with the pattern of changes produced by parathyroid hormone. However, the source of the stimulus for hormone secretion was not apparent since plasma calcium concentrations showed no significant difference between paired studies. The implications of these findings relative to control of hormone secretion, calcium regulatory mechanisms, and metabolic bone disease are discussed.

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