Human chorionic gonadotropin (hCG) maintains the corpus luteum in early pregnancy. The specific mechanism is:

• A hCG shares the beta subunit with LH and binds LH/hCG receptors on luteinized granulosa cells, activating Gs/cAMP/PKA to maintain progesterone synthesis until the placenta takes over at 8–10 weeks (luteoplacental shift) ✓
• B hCG inhibits FSH secretion from the pituitary, preventing development of new follicles that would compete with corpus luteum function
• C hCG directly stimulates trophoblast cells to secrete progesterone, supplementing corpus luteum progesterone from implantation onward
• D hCG binds TSH receptors on corpus luteum cells, providing thyroid hormone-like stimulation that prolongs luteal function

Explanation

hCG is a glycoprotein hormone secreted by the syncytiotrophoblast starting 7–9 days after fertilization. It shares the alpha subunit (common to FSH, LH, TSH) with LH and has an identical beta subunit binding domain. hCG binds the same LH/hCG receptor (LHCGR) on luteal cells, activating the Gs-cAMP-PKA pathway to maintain steroidogenesis (especially progesterone) that prevents luteolysis and maintains the endometrium. hCG levels peak at 8–10 weeks and then fall as the placenta (trophoblast) takes over progesterone synthesis (luteoplacental shift) — rendering the corpus luteum dispensable. hCG also stimulates thyroid function (TSH receptor cross-reactivity) explaining gestational hyperthyroidism.

Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.