Type 2 diabetes is characterised by insulin resistance and islet beta cell dysfunction that together contribute to hyperglycaemia. However it is important to highlight that without a defect in islet function resulting in reduced insulin secretion diabetes does not ensue. There are a number of mechanisms that can contribute to islet beta cell dysfunction and understanding these will provide better therapeutic strategies in treating this disease. We have been working on the hypothesis that overworking the islet beta cell is deleterious to its function and survival long term and will provide pre-clinical and clinical evidence to support this theory. This is management implications as one of the classes of drugs commonly used to treat diabetes stimulate the islet beta cell to overwork. We have therefore suggested that “metabolic deceleration” is a reasonable strategy to protect the islet beta cell from destruction under conditions of excess nutrient exposure. Thus approaches that reduce the work-load on the islet beta cell must be considered in the long-term treatment of Type 2 diabetes.