SLC39A14 and serum lipopolysaccharide activity: In the research presented here, a novel murine Zip14−/− model was used to demonstrate that ablation of the ZIP14 zinc transporter prevented the hypozincemia produced by LPS administration and that ZIP14 is a key component for controlling altered zinc homeostasis and signaling pathways in multiple tissues, including liver, white adipose tissue (WAT) and muscle, during endotoxemia.