**11. Conclusions and perspectives**

Over-nutrition and diminished physical activity in the modern lifestyle has led to a staggering increase in T2DM onset in Western cultures [108]. However, the epidemic is also progressing into the developing world, indicating that T2DM has become a major global health issue [108]. Since the 1990's, T1DM has more than doubled in number and is expected to double again before 2020 [108,148]. The traditional classification of distinct criteria for T1 and T2DM syndromes has become blurred due to the global increase in obese individuals and the incidence of obesity-related insulin-resistance [108]. Currently the paradigm of T1 and T2DM treatment appears to be changing in line with the clarification of dysfunctional pathways that are common to both disease types. Although diet-and-exercise still remains the most effective (and cheapest) treatment, new therapies will be required going into the future. Consequently, an increased understanding of the molecular and biochemical mechanisms that lead to disease onset and progression are mandatory.

In this manuscript, we have examined some of the key pathways that are essential in the pathogenesis of both T1 and T2DM, and we have reviewed some of the novel treatments that are currently being developed to counteract these dysfunctional processes. It is clear that inflammation, generation of ROS/RNS and ER stress leads to significant damage to pancreatic β-cells, culminating in cell dysfunction, and ultimately cell death. It is hoped that further study of the NFκB and the ER stress-mediated pathways, will reveal novel therapeutic targets that can be developed into a new generation of anti-diabetic treatments, that will improve β-cell function, survival and regeneration in T1 and T2DM.
