To assess whether disruption of Slc39a5 function improves glycemic traits in mice, we challenged the Slc39a5-/- mice with well-established models of congenital (leptin-receptor deficiency; Lepr-/- mice) or diet-induced obesity (Huang et al., 2004; King, 2012). This evidence concerns the gene LEPR and hyperinsulinemic hypoglycemia, familial, 4.