Zinc is an essential trace element involved in a multitude of human biological processes. Normally, zinc homeostasis is largely maintained by uptake of zinc into the enterocyte involving the brush border membrane followed by baso-lateral membrane exit into the circulation. This is accomplished by distinct gene-based protein carriers (eg., ZIP4, ZnT-1) to balance zinc loss, particularly from the intestinal and urinary tracts as well as integument. A genetically-based autosomal recessive disorder, acrodermatitis enteropathica, and other disorders leading to secondary malabsorption of zinc, such as celiac disease, may alter this balance, lead to significant dermatologic and intestinal histological effects, but may be entirely reversible with oral zinc supplements. Importantly, zinc may also attenuate transglutaminase activities and has been suggested to have the potential, hypothetically, to promote the generation of “celiac-safe” products.

zinc, ZIP4 microvillus membrane transporter, ZnT-1 basolateral membrane transporter, enterocyte zinc homeostasis, acrodermatitis entero pathica, zinc absorption and malabsorption