Open Access eBooks is inviting researchers working in the areas of Type 2 Diabetes to submit their book chapter for the publication in volume 1 of an eBook entitled An eBook on Type 2 Diabetes
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Although the clear mechanism of T2DM is still to be elucidated, it has been well established that reactive oxygen species (ROS) derived from multiple sources plays a causal role in multiple types of insulin resistance and contributes to β-cell dysfunction thus enhances the development and progression of T2DM. What is incomprehensible is that the detrimental ROS also plays a substantial role in the normal insulin signal transduction and glucose-stimulated insulin secretion (GSIS) in β-cell, which forces us to re-recognize the role of ROS under physiological and pathological conditions in a more broad way. Redox homeostasis is tightly controlled by the transcriptional factor nuclear factor erythroid 2-related factor 2 (Nrf2), whose abnormality is believed to be related with diabetes. Accumulating evidences suggest that there are important cross-talks between Nrf2 and PPARγ, PGC1α, PI3K/Akt on regulating antioxidant enzymes and the development of diabetes. Therefore, these evidences indicate that Nrf2 may be a critical element in taking survival and death decisions when cells are exposed to an oxidant environment. In conclusion, enhancing GSIS and insulin sensitivity through the regulation of Nrf2 levels is a potential avenue for developing new therapeutics. Nrf2 may become a promising target for the treatment of T2DM.
Recent advances in the pathophysiology of Type 2 Diabetes have made tremendous progress in the development of new treatment modalities for Diabetes. These new treatment regimens have allowed clinicians to tailor fit medications according to their patients’ diabetes profile and phenotype. In my review publication on pharmacologic treatment options for Type 2 Diabetes published at the Mayo Clinic Proceedings in 1996, Tan et al emphasized that only three classes of oral medications were then available for our patients namely sulfonylureas, biguanides and alpha glucosidase inhibitors . Twenty years later, significant changes in the understanding of diabetes have resulted in newer and safer medications for our patients. The Ominous Octet physiology of Diabetes  have advanced our way of treating diabetics with monotherapy to early combination therapy using different agents acting on different mechanisms.
The pathophysiological mechanisms associated with chronic renal disease in type 2 diabetic are complex and still remain to be fully understood. It is well known that there are traditional factors responsible for kidney disease such as poor metabolic control, time of evolution of diabetes, age, gender, uncontrolled hypertension, ethnical background and genetic factors. Nevertheless, recent evidence also points to non-traditional risk factors that might trigger glomerular barrier changes, leading to an increase durinary album in excretion along side with the progression of diabetic nephropathy to end-stage chronic kidney disease. Among these factors are inflammation and oxidative stress; alterations in mineral metabolism and homeostasis might also contribute to the clinical manifestation and/or progression of diabetic nephropathy.