FSH vs LH

Binds FSH receptors on Sertoli cells in testes to support sperm maturation and inhibin B production. In women, binds granulosa cell FSH receptors to drive follicular growth and estradiol production.

FSH (follicle-stimulating hormone) is an endogenous heterodimeric glycoprotein hormone produced and secreted by pituitary gonadotrophs, composed of a non-covalently associated common alpha subunit shared with LH, TSH, and hCG, and a unique FSH-specific beta subunit that confers receptor specificity; it is the primary regulator of gametogenesis in both sexes, acting on ovarian granulosa cells and testicular Sertoli cells to drive reproductive development. FSH activates its cognate receptor (FSHR) through cAMP-mediated signaling to stimulate follicular maturation and estradiol synthesis in the ovary via aromatase upregulation, and to support spermatogenesis in the testis by promoting Sertoli cell function and germ cell proliferation; FSH levels rise dramatically at menopause as negative feedback from ovarian estrogen declines. A Cochrane systematic review and meta-analysis established that recombinant FSH preparations are clinically equivalent to urinary-derived gonadotropins for ovarian stimulation in assisted reproductive technology cycles, providing the evidence base underlying current ART practice; this review supports the use of recombinant FSH as the standard of care for controlled ovarian hyperstimulation. FDA-approved recombinant FSH preparations — follitropin alfa (Gonal-f) and follitropin beta (Follistim) — require a prescription and are indicated for ovulation induction and ART in women and for hypogonadotropic hypogonadism in men; endogenous FSH is not administered as a therapeutic agent, and research-grade recombinant FSH is used as a cell culture tool and reproductive biology research compound.

Binds LH receptors on testicular Leydig cells, stimulating the cholesterol → testosterone biosynthetic pathway. In women, the LH surge triggers ovulation and supports luteal phase progesterone production.

LH (luteinizing hormone) is an endogenous heterodimeric glycoprotein hormone produced by pituitary gonadotrophs, sharing the common alpha subunit with FSH, TSH, and hCG, with a unique LH-beta subunit structurally homologous to hCG-beta; LH drives sex steroid synthesis through pulsatile release regulated by hypothalamic GnRH, and mediates the midcycle LH surge that triggers ovulation in women and sustains Leydig cell testosterone production in men. LH activates its receptor (LHR/LHCGR) on ovarian theca cells to stimulate androgen synthesis (which granulosa cells aromatize to estrogen under FSH regulation) and triggers follicular rupture and corpus luteum formation during the ovulatory surge; in men, tonic LH stimulates Leydig cell testosterone biosynthesis through cAMP/StAR pathway activation. A double-blind randomized controlled trial of supplemental recombinant LH (lutropin alfa) during controlled ovarian stimulation for ART demonstrated comparable clinical outcomes to FSH-only protocols in patients with baseline LH deficiency, providing evidence that lutropin alfa can serve as an effective LH substitute in gonadotropin-deficient women undergoing fertility treatment. Lutropin alfa (Luveris; Pergoveris in co-formulation with FSH) is approved in the European Union and several other jurisdictions for stimulation of follicular development in women with profound LH deficiency, but is not broadly approved in the United States; endogenous LH is not used as a therapeutic agent, and hCG — structurally similar to LH with a longer plasma half-life — is typically used as an LH surrogate for ovulation triggering and luteal phase support in US clinical practice.