The essential micronutrient zinc (Zn2+) plays an important role in many biological processes like growth, development, and reproduction. It is found in the active site of many enzymes, where ionization, polarization or replacement of Zn2+ bound water is involved in catalytic reactions. As a charged ion Zn2+ cannot cross biological membranes by simple diffusion and must be transported by specialized transport mechanisms. Two families of Zn2+ transporters, SLC30 (ZnT, Zn2+ transporter) and SLC39 (ZIP, Zinc (Zn2+)-Iron (Fe2+) permease), function in opposite directions to maintain cellular Zn2+ homeostasis (1).
Ten Zn2+ transporter proteins ZnT1-10 have been described. All of them contain several transmembrane domains and a histidine rich intracellular loop (2).
ZnT1 is abundantly expressed and has been suggested to be responsible for the efflux of Zn2+ from cells. It is upregulated by high oral Zn2+ doses. ZnT1 plays an essential role in maintaining neuronal Zn2+ balance, which is critical for synaptic signalling, neuroprotection, and the prevention of Zn2+ toxicity. Dysregulation of ZnT1 in neural tissues has been linked to neurodegenerative conditions and cognitive impairments (3). ZnT1 is involved in regulating Zn2+ levels within β-cells, which is essential for insulin storage and secretion. Proper ZnT1 function ensures optimal pancreatic endocrine activity and supports glucose homeostasis (4).