Type 1 diabetes (T1D) is a severe chronic condition that usually presents in young children. It is characterised by hyperglycaemia due to destruction of the insulin-producing beta cells in pancreatic islets. Islet transplants have the potential to cure T1D, however, currently they only have an 11% percent long-term success rate. Developing ways to protect transplanted islets from failure would be a major step towards a real cure. Preliminary data suggests that Metformin, a common type 2 diabetes drug, can protect beta cells and improve their function. While Metformin is known to act on liver cells, its mechanisms of protecting beta cells is unknown. The aim of this study was to investigate whether the known effects of Metformin in liver cells play a role in its ability to protect beta cells. INS-1E cells, an immortalised rat beta cell line, were cultured under low or high glucose conditions to mimic a normal and diabetic environment respectively, and treated with and without Metformin. Metformin protected beta cells in diabetic conditions and this was associated with activation of the 5' adenosine monophosphate-activated protein kinase (AMPK) pathway as is seen in liver cells and activation of protein kinase-A (PKA), opposing what was found in liver cells. However, altered expression of metabolic enzymes seen in liver cells, did not occur in beta cells. The AMPK and PKA pathways may be important mediators of Metformins effects in beta cells. Further studies will investigate its role in transplanted islets.