
Intracellular zinc signaling via Krüppel-like transcription factor 6 promotes HuD expression in pancreatic β cell
Dysfunction of pancreatic β cells caused by zinc deficiency is related to the pathogenesis of diabetes.1 Impaired zinc homeostasis in diabetes is associated with reduced zinc transporters.2 Down-regulation of HuD, an essential factor for normal β cell function, has been shown in diabetes.3 To assess the correlation between cellular zinc level and HuD expression in diabetes, relative levels of HuD and ZIP8, a highly expressed Zrt-, Irt-like protein (ZIP) transporter protein in β cells,4 were analyzed between db/db mice and control wild-type mice. HuD and ZIP8 expressions were down-regulated in the pancreas of db/db mice compared with that in control mice (Fig. 1A, B). Cellular zinc content was also reduced in pancreatic islets of db/db mice (Fig. 1B). These results suggest a positive correlation between intracellular zinc contents and HuD expression in the islet of the pancreas.