Department of Endocrinology, Aarhus University Hospital, Tage-Hansensgade, DK-8000 Aarhus C, Denmark.
Diabetologia. 2010 Aug;53(8):1549-51. doi: 10.1007/s00125-010-1793-x. Epub 2010 May 21.
The role of zinc in islet function has recently achieved new attention as a consequence of the identification of zinc transporter 8 (ZNT8) in islets, and the association of mutations in the gene for this zinc transporter with glucose intolerance and type 2 diabetes. ZNT8 is also an autoantigen associated with the appearance of type 1 diabetes. A number of experimental models have been employed to suggest how ZNT8 and other zinc transporters regulate beta cell insulin processing and possibly secretion. An additional role for the zinc transporters in regulating alpha cell function has been suggested. In this issue of Diabetologia, Wijesekara and colleagues, using a cell-specific Znt8 (also known as Slc30a8) knockout model, demonstrate that beta cell insulin processing and glucose tolerance is negatively affected after beta cell knock out of Znt8, whereas Znt8 knockout in alpha cells seems to have little effect on glucagon secretion or glucose tolerance. Although we are yet to see the therapeutic potential of these new findings, the area represents a field through which manipulation of islet function may eventually be possible.
锌在胰岛功能中的作用最近受到了新的关注，这是由于锌转运体 8（ZNT8）在胰岛中的鉴定，以及该锌转运体基因的突变与葡萄糖耐量异常和 2 型糖尿病的关联。ZNT8 也是与 1 型糖尿病出现相关的自身抗原。一些实验模型被用来提示 ZNT8 和其他锌转运体如何调节β细胞胰岛素的加工和分泌。锌转运体在调节α细胞功能方面可能还有其他作用。在本期《糖尿病学》中，Wijesekara 及其同事使用细胞特异性 Znt8（也称为 Slc30a8）敲除模型表明，β细胞敲除 Znt8 后β细胞胰岛素加工和葡萄糖耐量受到负面影响，而α细胞敲除 Znt8 对胰高血糖素分泌或葡萄糖耐量似乎影响不大。尽管我们还没有看到这些新发现的治疗潜力，但该领域代表了一个可以通过操纵胰岛功能最终实现的领域。
