The infant of a diabetic mother (IDM) represents a clinical model of fetal programming and in utero metabolic disease. Chronic maternal hyperglycemia drives fetal beta-cell hyperplasia through the Pedersen hypothesis: maternal glucose crosses the placenta, stimulating fetal insulin secretion. Insulin acts as a fetal growth hormone, promoting anabolic pathways including glycogenesis, lipogenesis, and protein synthesis, resulting in macrosomia and organomegaly. At birth, abrupt cessation of transplacental glucose delivery combined with persistent hyperinsulinism produces severe hypoglycemia within 1-4 hours. The metabolic cascade extends beyond glucose: insulin suppresses fetal parathyroid hormone (causing hypocalcemia at 24-72 hours), chronic fetal hypoxia from placental insufficiency stimulates erythropoietin (causing polycythemia and subsequent hyperbilirubinemia), and insulin antagonizes cortisol-mediated surfactant production (increasing RDS risk even at term). Hypertrophic cardiomyopathy occurs in 30% of IDMs from glycogen deposition in the interventricular septum, typically resolving within weeks as insulin levels normalize. The clinician prescribes glucose management protocols, manages the full metabolic panel, coordinates diagnostic evaluation, and guides the transition to outpatient follow-up.