Studies have demonstrated that susceptibility to type 2 diabetes (T2D) is influenced by common polymorphism in the zinc transporter 8 gene SLC30A8, providing novel insight into the role of zinc in diabetes. Intriguingly, zinc participates in every step of the process, including insulin synthesis, crystallization, storage, secretion and signaling. Zinc deficiency or overload is associated with various disorders, such as diabetes, cardiovascular disease and obesity. Zinc supplementation is considered as an effective means of treating or preventing T2D in people with certain SLC30A8 genotypes. Three important protein families-zinc transporters (ZnTs), zinc importers (ZiPs) and metallothionein (MT)-participate in maintaining zinc homeostasis. Here, we review research on the physiological characteristics of zinc and its role in the pancreas and homeostasis regulation mechanisms, along with the latest research on the structure and function of ZnT/ZiP and MT. In addition, we summarize the advancements in research on SLC30A8 gene polymorphism in search of a mechanism to explain the relationship between the R risk allele and zinc transporter activity.
Keywords: Diabetes; Pancreas; Zinc; Zinc regulators; ZnT8.