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Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc
digestion. Digestion produces the opportunity for zinc to bind to exogenous and endogenous constituents in the intestinal lumen, including peptides, amino acids, nucleic acids, and other organic acids and inorganic anions such as phosphate. The vast majority of zinc is absorbed by the small intestine through a transcellular process with the jejunum being the site with the greatest transport rate (Cousins, 1989b; Lee et al., 1989; Lonnerdal, 1989).
Absorption kinetics appear to be saturable, and there is an increase in transport velocity with zinc depletion. Paracellular transport may occur at high zinc intakes. Transit time also influences the extent of absorption to an extent that, in malabsorption syndromes, zinc absorption is reduced. Transfer from the intestine is via the portal system with most newly absorbed zinc bound to albumin.
Considerable amounts of zinc enter the intestine from endogenous sources. Homeostatic regulation of zinc metabolism is achieved principally through a balance of absorption and secretion of endogenous reserves involving adaptive mechanisms programmed by dietary zinc intake (King and Keen, 1999). Zinc depletion in humans is accompanied by reduced endogenous zinc loss on the order of 1.3 to 4.6 mg/day, derived from both pancreatic and intestinal cell secretions. Strong evidence suggests zinc transporter proteins in the various tissues act in concert to obtain such adaptation, but evidence is lacking in humans (McMahon and Cousins, 1998).
Measurement of true absorption, which eliminates the contribution of endogenous zinc from calculations, shows that zinc depletion increases the efficiency of intestinal zinc absorption. Regulation of absorption may provide a “coarse control” of body zinc, whereas endogenous zinc release provides “fine control” to maintain balance (King and Keen, 1999). An autosomal recessive trait, acrodermatitis enteropathica, is a zinc malabsorption problem of undetermined genetic basis. The mutation causes severe skin lesions and cognitive dysfunction (Aggett, 1989). The genetic defect suggests that one gene has a major influence on zinc absorption.
Tracer studies have shown that zinc is metabolically very active with initial uptake by liver representing a rapid phase of zinc turnover. Over 85 percent of the total body zinc is found in skeletal muscle and bone (King and Keen, 1999). While plasma zinc is only 0.1 percent of this total, its concentration is tightly regulated at about 10 to 15 μmol/L. Stress, acute trauma, and infection cause changes in hormones (e.g., cortisol) and cytokines (e.g., interleukin 6) that lower plasma concentration. Small changes in tissue pools could cause the decrease. In humans, plasma zinc concentrations are maintained without notable change when zinc intake is restricted