Pregnancy induces progressive insulin resistance as a physiological adaptation to ensure continuous glucose delivery to the growing fetus. In early pregnancy (first trimester), maternal insulin sensitivity actually increases slightly due to rising estrogen and progesterone, which enhance pancreatic beta-cell proliferation and insulin secretion. This increased sensitivity, combined with fetal glucose consumption, predisposes to fasting hypoglycemia — particularly dangerous in pre-existing type 1 diabetes where insulin doses may need reduction by 10–20% in the first trimester. By mid-to-late pregnancy (24–28 weeks), placental hormones — primarily human placental lactogen (hPL), cortisol, progesterone, prolactin, and TNF-alpha — create profound insulin resistance. hPL has anti-insulin and lipolytic properties, increasing maternal free fatty acid availability while redirecting glucose to the fetus. Insulin requirements may double or triple compared to pre-pregnancy levels. In women with adequate pancreatic reserve, compensatory hyperinsulinemia maintains euglycemia. When beta-cell function cannot meet the increased demand, gestational diabetes (GDM) or worsening of pre-existing diabetes occurs. Glucose crosses the placenta by facilitated diffusion via GLUT1 transporters. Maternal hyperglycemia directly causes fetal hyperglycemia, stimulating fetal pancreatic beta-cell hyperplasia and hyperinsulinemia. Fetal insulin acts as...