Type 1 diabetes mellitus (T1DM) is an autoimmune disease in which autoreactive CD4+ and CD8+ T lymphocytes infiltrate the pancreatic islets of Langerhans and selectively destroy insulin-producing beta cells. This insulitis is mediated by autoantibodies including anti-glutamic acid decarboxylase (anti-GAD65), anti-islet cell antibodies (ICA), anti-insulin antibodies (IAA), and anti-zinc transporter 8 (ZnT8). The destruction is gradual, with clinical diabetes manifesting when approximately 80-90% of beta-cell mass is lost, resulting in absolute insulin deficiency. Without insulin, glucose cannot enter insulin-dependent tissues, leading to hyperglycemia, uninhibited lipolysis, hepatic ketogenesis, and diabetic ketoacidosis (DKA) with anion gap metabolic acidosis. Type 2 diabetes mellitus (T2DM) is characterized by progressive insulin resistance in skeletal muscle, liver, and adipose tissue, combined with relative beta-cell dysfunction. Insulin resistance results from post-receptor signaling defects in the PI3K/Akt pathway, often driven by chronic caloric excess, visceral adiposity, and pro-inflammatory cytokines (TNF-alpha, IL-6) secreted by adipose tissue. Initially, beta cells compensate with hyperinsulinemia, but over time beta-cell exhaustion occurs through glucotoxicity and lipotoxicity, leading to amyloid polypeptide (IAPP) deposition in islets and progressive beta-cell apoptosis. Hepatic insulin resistance causes inappropriate...