The aim of this paper is to review the information on type 1 and type 2 diabetes with emphasis on its etiology, pathogenesis and pathophysiology via literature review. Diabetes is a group of metabolic disorders characterized by a chronic hyperglycemic condition resulting from defects in insulin secretion, insulin action or both. Type 1 diabetes is the result of an autoimmune reaction to proteins of the islets cells of the pancreas while type 2 diabetes is caused by a combination of genetic factors related to impaired insulin secretion, insulin resistance and environmental factors such as obesity, overeating, lack of exercise and stress, as well as aging. The pathogenesis of selective β-cell destruction within the islet in type 1 diabetes mellitus is difficult to follow due to marked heterogeneity of the pancreatic lesions. At the onset of overt hyperglycemia, a mixture of pseudoatrophic islets with cells producing glycogen, somatostatin and pancreatic polypeptide, normal islets and islets containing both β-cells and infiltrating lymphocytes and monocytes may be seen. The autoimmune destruction of pancreatic β cells leads to a deficiency of insulin secretion that leads to the metabolic derangements associated with type 1 diabetes. The main pathophysiological features of type 2 diabetes are impaired insulin secretion and increased insulin resistance. The impairment of pancreatic β cell function notably shows progression overtime in type 2 diabetes although aging, obesity, insufficient energy consumption, alcohol drinking, smoking, etc are independent risk factors of pathogenesis of type 2 diabetes mellitus.