Zn2+ toxicity is implicated in pancreatic β-cell death that occurs secondarily to: streptozotocin exposure in vitro and both autoimmune attack or streptozotocin in vivo models of T1DM. Type-1 diabetes (T1DM) is an autoimmune disease resulting from specific T-lymphocyte-, ROS-, and cytokine-mediated destruction of the insulin-producing β-cells of the islets of Langerhans resulting in dysregulation of blood glucose. The development of T1DM is reduced by treatment with T-cell and cytokine inhibitors, and ROS scavengers. These oxidative processes are suggested to alter the NAD+/ NADH ratio and inhibit proteins involved in energy metabolism and glycolysis causing the accumulation of triosephosphates. Inhibitors of NAD+ catabolism have been demonstrated to attenuate diabetic incidence in models of T1DM. NAD+ loss is linked to diabetes. Heterozygous knockout of the rate limiting enzyme in NAD+ synthesis (Nampt), causes reduced insulin secretion. Also, Nampt and NAD+ levels are reduced in T2DM and the aging or high-fat diet models thereof. Restoration of NAD+, by nicotinamide mononucleotide precursor supplementation, attenuates diabetes in aging and high-fat diet mouse models of T2DM.