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Updated: Oct 16, 2026

Atomic Absorbance Spectroscopy to Measure Intracellular Zinc Pools in Mammalian Cells
Published on: May 16, 2019
Overview of zinc absorption and excretion in the human gastrointestinal tract
1Section of Nutrition, Department of Pediatrics, University of Colorado School of Medicine, Denver, CO 80262, USA.
Abstract:
Zinc homeostasis is primarily maintained via the gastrointestinal system by the processes of absorption of exogenous zinc and gastrointestinal secretion and excretion of endogenous zinc. Although these processes modulate net absorption and the size of the readily exchangeable zinc pools, there are limits to the effectiveness of the homeostatic mechanisms of these and other systems. As a result of the interplay of the subcellular regulation of these mechanisms and host, dietary and environmental factors, zinc deficiency is not uncommon, especially on a global basis. This overview briefly reviews current understanding about the subcellular mechanisms of zinc absorption and transport. Factors recognized to affect zinc absorption at the whole body level are reviewed and include the amount and form of zinc consumed; dietary promoters, such as animal protein and low-molecular-weight organic compounds; dietary inhibitors, such as phytate and possibly iron and calcium when consumed as supplements; and physiologic states, such as pregnancy, lactation and early infancy, all of which increase the demand for absorbed zinc. The control of endogenously secreted zinc is less well understood. Available data suggest that the quantity of secreted zinc with each meal may be considerable and that efficient reabsorption is critical to the maintenance of normal zinc balance. Factors that have been proposed to interfere with the normal reabsorption of endogenous zinc include phytate and unabsorbed fat. Understanding of the dietary, physiologic, pathologic and environmental factors that may adversely affect these processes, and therefore zinc homeostasis, will be critical to preventing and treating zinc deficiency in human populations.
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