Luteinizing hormone (LH)
Also known as: LH, lutropin, interstitial cell-stimulating hormone, ICSH
A glycoprotein gonadotropin that stimulates testosterone production by Leydig cells and androgen production by theca cells; its mid-cycle surge triggers ovulation and formation of the corpus luteum.
Overview
LH acts on the LH/choriogonadotropin receptor (LHCGR), a Gs-coupled GPCR that also binds hCG. In the testis it stimulates Leydig cells to convert cholesterol to testosterone (via StAR and CYP11A1), the high local concentration of which is essential for spermatogenesis. In the ovary it stimulates theca interna cells to produce androstenedione, which diffuses to granulosa cells for aromatisation to estradiol.
The LH surge — triggered when estradiol from the dominant follicle stays above a threshold (≈200 pg/mL) for ≈36–48 h and switches feedback from negative to positive — lasts about 48 h. It causes the oocyte to resume and complete meiosis I (forming the secondary oocyte and first polar body), expansion of the cumulus, production of prostaglandins and proteolytic enzymes that rupture the follicle wall, and luteinisation of granulosa and theca cells. Ovulation follows ≈24–36 h after the surge begins (≈10–12 h after its peak). LH then maintains the corpus luteum through the luteal phase.
- Location
Source: gonadotrophs of the anterior pituitary. Targets: Leydig cells (testis); theca cells, mature granulosa cells and corpus luteum (ovary).
Function
- Stimulates testosterone synthesis by Leydig cells.
- Stimulates theca-cell androgen synthesis (estrogen precursor).
- Mid-cycle surge triggers resumption of meiosis, ovulation and luteinisation.
- Maintains progesterone secretion by the corpus luteum.
- Physiology
Class: glycoprotein (α + β). Receptor: LHCGR — Gs/cAMP. Half-life ≈20–30 min.
- Regulation
Stimulated by fast-frequency GnRH pulses; inhibited by testosterone, estradiol and progesterone (negative feedback); sustained high estradiol produces positive feedback and the surge.
Clinical significance
Ovulation prediction
Urinary LH kits detect the surge, indicating ovulation within ≈24–36 h — the most fertile window.
PCOS
Rapid GnRH pulse frequency increases LH relative to FSH; LH-driven theca androgen excess contributes to hyperandrogenism and arrested follicle development.
Hypogonadism
Low testosterone with high LH = primary testicular failure (e.g. Klinefelter); low testosterone with low/normal LH = secondary (pituitary/hypothalamic) hypogonadism.
Compiled from standard anatomy and physiology references — see the Endocrine System sources. For education only; not medical advice.