Type 1 vs Type 2 Diabetes — Pathophysiology

Type 1 diabetes is an autoimmune destruction of pancreatic beta cells, resulting in absolute insulin deficiency. The immune system attacks the islets of Langerhans, leaving the pancreas unable to produce insulin at all. Without exogenous insulin, the client cannot move glucose into cells and will break down fat for fuel — which is why Type 1 presents acutely, often with DKA as the first sign. Onset is typically in childhood or young adulthood, though it can occur at any age. Autoantibodies (such as GAD65 and islet cell antibodies) confirm the autoimmune process. Type 2 diabetes begins with insulin resistance: cells have functioning insulin receptors but impaired post-receptor intracellular signaling (e.g., reduced GLUT4 translocation) blunts insulin's effect. The pancreas compensates by overproducing insulin (hyperinsulinemia), but over years the beta cells exhaust and insulin production declines — a progressive loss, not a sudden one. Because some insulin is still present, lipolysis is partially suppressed, so Type 2 rarely presents with DKA (though ketosis-prone Type 2 can occur, especially in African American and Hispanic populations). Instead, Type 2 accumulates hyperglycemia gradually and may present with HHS rather than DKA. Risk factors for Type 2 include obesity, sedentary lifestyle, and metabolic syndrome. Type 1 always requires exogenous insulin from diagnosis; Type 2 typically begins with lifestyle modification ± metformin. Diagnosis is confirmed by fasting glucose ≥126 mg/dL, A1C ≥6.5%, or random glucose ≥200 mg/dL with symptoms. C-peptide levels help differentiate: low or absent in Type 1, normal or elevated in early Type 2.