This disclosure relates to a rodent model. More specifically, this disclosure relates to a loss of function of solute carrier 39 member 5 (SLC39A5) rodent model. In particular, disclosed herein are genetically modified rodent animals that carry a loss of function mutation in an endogenous Slc39a5 gene and use of such rodent animals in elucidating the role of SLC39A5 in zinc homeostasis, glycemic regulation and lipid metabolism.