Histopathological changes in the diabetic pancreas are characterized by several key alterations that impact its structure and function. In type 1 diabetes mellitus (T1DM), autoimmune destruction of insulin-producing beta cells within the pancreatic islets results in their selective loss, termed insulitis. This process involves infiltration of immune cells such as T lymphocytes and macrophages into the islets, leading to progressive beta cell destruction and ultimately insulin deficiency. In contrast, type 2 diabetes mellitus (T2DM) is associated with insulin resistance and eventual beta cell dysfunction and depletion. Histologically, T2DM pancreases often show features of islet hypertrophy, where individual islets increase in size in response to chronic hyperglycemia and insulin resistance. Moreover, deposition of amyloid protein within the islets, known as islet amyloidosis, is commonly observed in T2DM and can contribute to beta cell dysfunction. These histopathological changes reflect the complex interplay of genetic, environmental, and metabolic factors in the pathogenesis of diabetes and highlight the importance of understanding pancreatic pathology for developing targeted therapies and interventions.