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Solute carrier family 39 member 5 (SLC39A5), commonly known as ZIP5, is a zinc transporter belonging to the ZIP family responsible for zinc influx across the basolateral membrane of polarized cells, particularly in intestinal enterocytes and pancreatic acinar cells[1][2][3][4]. It plays a central role in the homeostasis of zinc by mediating zinc excretion from the bloodstream into the intestine and regulating zinc levels in multiple tissues. SLC39A5 is essential in protecting the pancreas from zinc toxicity and facilitating normal zinc balance in the body—its expression is dynamically regulated according to zinc availability. Clinically, SLC39A5 mutations are linked to dominantly inherited high myopia (MYP24) and may have emerging roles in metabolic trait modulation, such as influencing type 2 diabetes risk via the regulation of serum zinc levels[2][4]. Loss of SLC39A5 function disrupts zinc distribution, leading to increased hepatic zinc and altered pancreatic zinc accumulation, especially under varying dietary conditions. No highly selective drugs are described for clinical use against this transporter, but genetic variants are under investigation as biomarkers for disease susceptibility and metabolic traits.
Modulation of zinc transport to alter intracellular and tissue zinc concentrations
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