Type 2 diabetes is an emerging epidemic affecting millions worldwide. It is a progressive disease characterised by increasing levels of glucose in the blood caused by the development of cellular resistance to insulin and decrease in beta cell function. Zinc is an important trace element shown to play an important structural and functional role in the endocrine hormone insulin. Zinc transporters play an essential role in transporting zinc into insulin secretory vesicles. Aim. To investigate the zinc and zinc transporter regulation in a leptin deficient type 2 diabetic db/db mice model compared to the age matched control (C57BL6J) mice. Methods. Zinc was measured using flame atomic absorption spectrometry 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 livers at 14 weeks showed significant reduction of zinc concentration compared to its age matched controls livers (49%, p<0.05, n=5). Db/db mice pancreas also showed significant reduction in zinc in the early diabetic mice (55%, p<0.05 n=6), diabetic (40%, p=0.0013, n=6) and chronic diabetic (26%, p=0.002,n=5) respectively compared to its aged matched controls. Zinc concentration in the plasma of the db/db mice were elevated compared to the controls. Pancreatic islets of 4, 10 and 18 weeks mice showed down regulation of efflux transporter ZnT8 and upregulation of influx transporter ZIP14 when counterstained with glucagon. Conclusion. The subcellular distribution of the zinc transporters ZnT8 and ZIP14 in 4, 10 and 18 week old mice db/db mice pancreas is altered during the progression of diabetes thereby affecting the zinc availability and regulation. Further experiments will be carried to investigate the regulation of these transporters using quantitative real time PCR.