Antidiabetic Agents: Pathophysiology of Diabetes Mellitus and Therapeutic Approaches

Diabetes mellitus is a heterogeneous group of chronic metabolic disorders characterized by hyperglycaemia resulting from defects in insulin secretion, insulin action, or both. Its pathophysiology involves a complex interplay between genetic susceptibility, autoimmunity, insulin resistance, β‑cell failure, chronic inflammation, oxidative stress, and environmental and lifestyle factors, ultimately leading to microvascular and macrovascular complications. Understanding these mechanisms provides the biological rationale for current and emerging antidiabetic therapies. This review summarizes the classification and pathophysiology of major diabetes subtypes, highlights key molecular and inflammatory pathways, and discusses pharmacological antidiabetic agents—including metformin, insulin secretagogues, thiazolidinediones, α‑glucosidase inhibitors, DPP‑4 inhibitors, GLP‑1 receptor agonists, SGLT2 inhibitors, insulin, and newer multi‑incretin agonists—in the context of underlying disease mechanisms and clinical outcome data. (1–3)