Zinc is an important trace element shown to play an important structural and functional role in pancreas being required by endocrine islet cell for insulin secretion and by exocrine acinar cells as pancreatic juice component^{1, 2}. ZnT8 is a member of the SLC30A family of zinc transporters involved packaging and secretion insulin in response to glucose, suggesting a possible role in regulating glycemia. ZnT8 in studies identified polymorphisms in the ZnT8 gene conferring increased during post transplantation diabetes^{1, 2}.Our study aims to investigate the zinc and zinc transporter regulation in a type 2 diabetic db/db mice model compared to age matched control (C57BL6J) mice. Methods. Zinc was measured using flame atomic absorption spectrometry and ZINPYR-1 staining (granular zinc) and immunofluorescence was done using frozen sections of pancreas of control and diabetic mice and were stained using zinc transporter antibodies. Results. Db/db mice pancreas showed significant reduction in zinc in the early diabetic mice (55%, p<0.05, n=6), diabetic (40%, p<0.05, n=6) and chronic diabetic (p=0.07, n=5) respectively compared to its aged matched controls. There was significant downregulation of zinc transporter ZnT8 and ZIP4 as early as 4 weeks and upregulation of transporter ZIP14 and there were no significant change in ZIP5 and ZnT7 protein expression when counterstained with glucagon. No significant change in gene expression of ZnT8 (p>0.05, n=6) ZIP4 (p>0.05, n=6), ZIP5 (p>0.05, n=6) and ZIP14 (p>0.05, n=6) were observed in db/db mice compared to controls in qRT-PCR. Conclusion. The subcellular distribution of zinc transporters ZnT8, ZIP5 and ZIP14 in 4, 10 and 18 week old mice db/db mice pancreas was altered in early age thereby reducing zinc availability for the maturation and release of insulin. Overexpression of one or more zinc transporters could potentially increase the insulin secretion capacity and cell viability with zinc supplementation and could be beneficial for islet cell transplantation.