This paper reviews 15 articles about nitric oxide`s role in FFA-induced apoptosis/cell death of â-cells in relation to DM2. These are mostly in vitro studies, but also included are 3 in vivo experiments. The main objects are to see if nitric oxide is a mediator in FFA-induced apoptosis/cell death, and if mechanisms are the same as in cytokine-induced apoptosis, like in Diabetes type 1. Results: In all the reviewed studies it is demonstrated that FFAs induce apoptosis, in vitro by exposing cells and islets to FFAs, as well as in vivo by measuring apoptosis in islets of obese rats and islets of wild-type rats. It is also shown in vitro that unsaturated fatty acids are less cytotoxic to â-cells than saturated fatty acids, by inducing little or no cell death. After exposure to FFAs, cells and islets accumulated triglycerides. In vivo studies showed that administration of iNOS inhibitors prevent DM2 and â-cell loss in ZDF rats. Several in vitro studies showed that FFAs induce NO production via iNOS and that iNOS inhibitors attenuate cytotoxic effects of FFAs, whereas other studies showed no such effects. Conclusion: FFAs induce apoptosis in â-cells and pancreatic islets. Saturated FFAs are more cytotoxic to â-cells and islets than unsaturated FFAs. FFAs induce accumulation of triglycerides in â-cells and islets. NO may be a mediator of FFA-induced apoptosis in â-cells, but does not seem to have the exact same induction pathways and damage methods as in cytokine-induced apoptosis.