| abstract |
The present disclosure relates to a rodent model. More specifically, the present disclosure relates to a loss-of-function rodent model of solute transporter 39 member 5 (SLC39A5). In particular, the use of genetically modified rodents with loss-of-function mutations in the endogenous Slc39a5 gene and such rodents in elucidating the role of SLC39A5 in zinc homeostasis, glycemic control and lipid metabolism is disclosed herein. To. |