Diabetes mellitus is a group of metabolic diseases characterized by hyperglycemia resulting from defects in insulin secretion, insulin action, or both. Type 1 DM (5-10%) is an autoimmune destruction of pancreatic beta cells mediated by T-lymphocytes and autoantibodies (anti-GAD, anti-IA2, anti-insulin), resulting in absolute insulin deficiency. The destruction occurs over months to years before clinical presentation, which typically occurs when >80% of beta cells are destroyed. Without insulin, glucose cannot enter cells, leading to intracellular starvation despite hyperglycemia, and the body catabolizes fat through lipolysis, producing ketone bodies (acetoacetate, beta-hydroxybutyrate, acetone) that cause metabolic acidosis (DKA). Type 2 DM (90-95%) involves insulin resistance in skeletal muscle, liver, and adipose tissue combined with progressive beta cell dysfunction. Insulin resistance requires compensatory hyperinsulinemia; when beta cells can no longer meet demand, hyperglycemia develops. Chronic hyperglycemia causes microvascular damage through: advanced glycation end products (AGEs), activation of protein kinase C, increased polyol pathway flux, and oxidative stress—leading to retinopathy, nephropathy, and neuropathy. Macrovascular disease (CAD, stroke, PVD) is accelerated by associated dyslipidemia and hypertension.