Gestational diabetes mellitus (GDM) results from the progressive insulin resistance of normal pregnancy becoming uncompensated in women with insufficient beta-cell reserve. During pregnancy, the placenta produces hormones — human placental lactogen (hPL), progesterone, cortisol, and placental growth hormone — that antagonize insulin action at the post-receptor level by interfering with insulin receptor substrate (IRS) phosphorylation and GLUT4 transporter translocation. This physiological insulin resistance serves an evolutionary purpose: redirecting maternal glucose across the placenta to the fetus via facilitated diffusion through GLUT1 transporters. In normal pregnancy, maternal beta cells undergo compensatory hyperplasia (30-50% increase in mass) driven by prolactin and hPL signaling, increasing insulin secretion 2-3 fold to maintain euglycemia. When beta-cell compensation is inadequate, maternal hyperglycemia develops, typically manifesting in the late second or third trimester when placental hormone production peaks. The oral glucose tolerance test (OGTT) exploits this pathophysiology: a 75-gram glucose load (IADPSG/WHO criteria) or two-step approach (50-gram glucose challenge test followed by 100-gram 3-hour OGTT using Carpenter-Coustan criteria) unmasks the impaired glucose disposal. Fetal consequences of maternal hyperglycemia include fetal hyperinsulinemia (fetal beta cells respond to transplacental...