Role of zinc in health and disease.
Level 5 - mechanism / opinion, no new human data
Narrative review describing physiological mechanisms and clinical conditions without systematic search methodology.
PubMed 38367035 · doi:10.1007/s10238-024-01302-6
What was done
This narrative review synthesizes the cellular, physiological, and clinical mechanisms of zinc homeostasis in humans. It outlines intestinal transport mechanisms, factors influencing bioavailability, bodily distribution, excretion pathways, inherited and acquired deficiency states, toxicity, and pharmacological interactions associated with oral zinc supplementation.
What was found
The abstract reports no quantitative empirical data or statistical estimates. It outlines key physiological pathways: dietary zinc absorption is mediated by transporters ZIP4 and/or ZnT5B in the duodenum, exported to circulation by ZnT1, and secreted into the lumen via ZnT5B. Absorption is enhanced by amino acids and citrate, but reduced by phytates, casein, and calcium. Approximately 70% of circulating zinc binds albumin, with bodily stores concentrated in skeletal muscle and bone. Excessive zinc impairs copper and iron absorption (causing deficiency and anemia), while deficiency stems from genetic mutations (such as SLC39A4 in acrodermatitis enteropathica), malabsorption, or medications (diuretics, angiotensin-receptor blockers). Oral zinc also reduces absorption of ciprofloxacin, doxycycline, and risedronate.
Why it matters
The review provides a consolidated reference on the physiological mechanisms of zinc handling, highlighting clinically relevant drug interactions, dietary inhibitors, and diagnostic contexts for both deficiency and excess.
Limits
The review is narrative and does not follow systematic review or meta-analytic methodology. No empirical participant sample size, quantitative effect sizes, or risk-of-bias assessments are reported in the abstract.
Cited by
- contradicts Excess copper intake, such as from copper plumbing pipes, depletes zinc in the body.