Pathophysiology of Type 2 Diabetes

While in the earlier times type 2 diabetes (T2D) was only considered as a disease related to a disturbance in the functioning of the pancreas, lots of evidences accumulated during the past few decades revealed a plethora of additional factors that contribute to this devastating disease. The understanding of T2D has evolved from recognizing the duo of pancreatic β-cell failure with defective insulin secretion and insulin resistance (IR), to the triumvirate with the addition of hepatic gluconeogenesis. Recently, the ominous octet (addition of deranged adipocyte metabolism, incretin defect, increased glucagon secretion, increased renal glucose reabsorption, and neurotransmitter dysfunction and central appetite dysregulation) and of later the dirty dozen (addition of dopamine, vitamin D, testosterone and renin-angiotensin system) elaborated on the prior simplistic disease models. Furthermore, with the addition of the gut, the unlucky thirteen, suggests that the contributing factors toward T2D pathogenesis are still in the process of being identified [1–9]. In this chapter, we will explore the various factors that have been identified or are being proposed as the underlying contributors to the pathogenesis and pathophysiology of T2D.