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Session II, Zinc in the GI Tract

Zinc and Health: Workshop Summary

Session II

Session II, Zinc in the GI Tract discussed the current knowledge of absorption, fractional absorption, and secretion, reabsorption, and the excretion of endogenous zinc in the GI tract. Regulation of bodily zinc homeostasis is complex and poorly understood. Complexity is apparent considering the mechanics of exchangeable zinc pools and their relationship to signaling to regulate processes at the whole body level, as well as relating to cellular processes of absorption.  A number of dietary factors influence the absorption of zinc to include phytate and certain minerals, particularly iron and calcium. Individual proteins can affect absorption in opposing directions.  Cellular zinc concentrations are maintained in large part due to zinc transporter proteins. Zinc transporter-1 (ZnT-1) proposed to serve as an exporter, is expressed in a variety of tissues, resides at the basolateral membrane of intestinal enterocytes and epithelial cells of the distal renal tubules and appears to function in integrative zinc acquisition and homeostasis. ZnT-2 and ZnT-3 may function in tissue specific vesicular zinc transport. ZnT-3 may be particularly important in Zn(II) packaging by synaptic vesicles. ZnT-4 is very abundant in mammary gland, and maybe associated with Zn secretion into milk.

Diarrhea and GI disease occur in a variety of environmental settings, where many factors play a role. Protein energy malnutrition and micronutrient deficiencies predispose to zinc deficiency conditions, however new strategies to redress these risks have been implemented and results of many international intervention studies were reviewed in this session.  Specific GI enzymes may be upregulated in zinc deficiency states and their mechanisms of action pose some very interesting questions about how zinc deficiency is related to the etiology of diarrhea and potentially the response to zinc supplementation during acute and persistent diarrhea.