Absence of <i>Slc39a14/Zip14</i> in mouse pancreatic beta cells results in hyperinsulinemia
Yu-Han Hung, Yongeun Kim, Samuel Blake Mitchell, Trista L. Thorn, Tolunay Beker Aydemir
Abstract
Metal transporter SLC39A14/ZIP14 is downregulated in pancreatic islets of patients with T2D and mouse models of HFD- or db/db-induced obesity. However, the function of ZIP14-mediated intracellular zinc trafficking in β cells is unknown. Our analyses revealed that SLC39A14 is the only Zn transporter expressed abundantly in human β cells besides SLC30A8. Within the β cells, ZIP14 is localized on the endoplasmic reticulum and serves as a negative regulator of insulin secretion, providing a potential therapeutic target for T2D.
Topics & Concepts
Endoplasmic reticulumHyperinsulinemiaPancreatic isletsSecretionCell biologyTransporterEndocrinologyIntracellularInternal medicineBiologyBeta cellRegulatorInsulinBETA (programming language)ChemistryIsletMedicineGeneInsulin resistanceBiochemistryComputer scienceProgramming languageTrace Elements in HealthIron Metabolism and DisordersPancreatic function and diabetes