The prevalence of type 2 diabetes (T2D) is increasing worldwide. This study provides essential information about the classification, diagnosis, pathogenesis, treatment, and complications of T2D. Glucose homeostasis is controlled by the rates of endogenous glucose production (EGP) and glucose utilization. EGP is ~2 mg/kg/min in humans and is equal to the rate of basal glucose utilization. During fasting, ~75-85% of EGP occurs in the liver and the remainder in the kidney. Hepatic glucose production is the main determinant of fasting blood glucose concentration. In the fed state, when insulin secretion is stimulated and glucagon secretion is inhibited, EGP decreases and glucose uptake in splanchnic (liver and gut) and peripheral (primarily muscle) tissues increases. β-cell dysfunction and insulin resistance represent core pathophysiological defects in T2D. Although the pathogenesis of T2D was previously focused on dysfunctions of "ominous triumvirate" (liver, skeletal muscle, and β-cell), it has been extended to "ominous octet," which includes defects in adipocytes (increased lipolysis), gastrointestinal tract (incretin deficiency/resistance), pancreatic α-cells (hyperglucagonemia), kidneys (increased glucose reabsorption), and brain (insulin resistance); endothelial dysfunction, inflammation, increased oxidative stress, and hypoxia are also involved in the pathogenesis of T2D. In conclusion, diabetes is one of the leading causes of morbidity and mortality worldwide. More insights into the pathophysiology of T2D necessitate revising the treatment approaches from only glycemic control to a pathophysiological-based view. In addition, new emerging complications of T2D such as cancer warrant further attention.