Abstract
Pancreatic acinar cells play an important role in zinc excretion. We have found that dietary Zn intake regulates the expression of ZnT1 and ZnT2 in the pancreas. The mechanisms with which ZnT1 and ZnT2 mediate Zn efflux in pancreatic acinar cells have not been characterized. Here, we report Zn deficiency caused a significantly lowered Zn concentration in both the cytoplasm and zymogen granule compartments of acinar cells. Western blot analysis also showed a decrease in the association of both ZnT1 and ZnT2 with the purified zymogen granule membrane fraction. In addition, in pancreatic AR42J cells, ZnT1 was found to be tightly regulated by intracellular Zn levels. In contrast, ZnT2 expression was upregulated by dexamethasone, which induces cell differentiation, and increases both secretory organelle development and secretion. Both ZnT1 and ZnT2 were down-regulated in Zn deficient cell cultures, obtained through the use of Zn chelating reagents, TPEN, DTPA, or dialysis against dipicolinic acid. In ZnT1 over-expressing transiently transfected AR42J cells, a lower intracellular Zn level and higher Zn efflux rate was found through 65Zn loss. Transient transfection of ZnT2 and over-expression resulted in more sequestered intracellular Zn, with a normal 65Zn efflux rate. In conclusion, ZnT1 and ZnT2 regulate Zn output through two different pathways in pancreatic acinar cells. Supported by NIH Grant DK 31127.
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