Luteinizing HormoneEdit
Luteinizing hormone (LH) is a key chemical messenger in the regulation of the reproductive systems of humans and other animals. It is produced by the anterior pituitary gland, a small but crucial gland at the base of the brain, and its secretion is governed by the hypothalamus through the releasing signal known as gonadotropin-releasing hormone (gonadotropin-releasing hormone). As a member of the gonadotropin family, LH acts on the gonads to stimulate the production of sex steroids and to induce ovulation in females, as well as supporting testosterone synthesis in males. LH, together with follicle-stimulating hormone (follicle-stimulating hormone), coordinates development, maturation, and function of the gonads across the life cycle. The molecule itself is a glycoprotein composed of alpha and beta subunits, with the beta subunit conferring receptor specificity and the alpha subunit shared with other pituitary glycoprotein hormones. The LH receptor (the Luteinizing hormone receptor) is a G protein–coupled receptor located on target cells in the ovary and testis, as well as on some other tissues in mammals.
Biology and Structure
LH belongs to the glycoprotein hormone family, which includes FSH and TSH. Its structure—an alpha subunit common to several hormones and a hormone-specific beta subunit—underpins its receptor recognition and biological activity. In humans, the LH receptor is expressed primarily on the ovarian theca cells and luteal cells in females, and on Leydig cells in the testes of males. Binding of LH to its receptor activates intracellular signaling pathways that raise intracellular cAMP, stimulate steroidogenesis, and promote luteinization of the follicle following ovulation. The general mechanism by which LH exerts its effects is highly conserved in mammals, and disruptions to LH signaling can have profound effects on fertility and puberty.
Cross-references: - anterior pituitary - hypothalamus - Luteinizing hormone receptor - Leydig cells - ovary - testis
Regulation of Secretion
LH secretion is pulsatile and tightly controlled by GnRH pulses from the hypothalamus. The frequency and amplitude of GnRH signaling shape the pattern of LH release, which in turn governs the timing of downstream events in the gonads. The sex steroids estrogen and progesterone provide feedback to the hypothalamus and pituitary: estrogen can exert negative feedback most of the cycle but switches to a positive feedback effect around the midcycle, producing the pre-ovulatory LH surge that triggers ovulation. After ovulation, progesterone from the corpus luteum exerts negative feedback to reduce further LH release. In males, LH pulses contribute to sustained testosterone production by the Leydig cells, which supports spermatogenesis and secondary sexual characteristics.
Cross-references: - GnRH - estrogen - progesterone - testosterone - ovulation
Physiological Roles
In females
In the female ovary, LH acts on the theca interna cells to stimulate synthesis of androgens, which are then aromatized to estrogens by the granulosa cells under the influence of FSH. The surge of LH at midcycle triggers ovulation—the release of a mature oocyte from the dominant follicle—and promotes luteinization, wherein the ruptured follicle transforms into the corpus luteum. The corpus luteum then secretes progesterone, with estrogen support, creating a hormonal environment suitable for potential pregnancy. Disruptions to LH signaling can contribute to disorders of ovulation and infertility.
Cross-references: - theca interna - granulosa cells - ovulation - corpus luteum - progesterone - estrogen
In males
In the male reproductive system, LH stimulates the Leydig cells to produce testosterone, which is essential for the development of male secondary sexual characteristics and for the initiation and maintenance of spermatogenesis. Adequate LH signaling is therefore important for normal reproductive function and fertility in men.
Cross-references: - Leydig cells - testosterone - spermatogenesis
Clinical Relevance
In fertility and assisted reproduction
LH has a central role in natural fertility cycles and is leveraged in assisted reproduction. The LH surge can be triggered clinically by administering human chorionic gonadotropin (human chorionic gonadotropin), which mimics LH activity to induce final oocyte maturation and ovulation in stimulated cycles. In some protocols, recombinant LH (rLH) is used in combination with FSH to optimize follicular development and steroidogenesis, particularly in women who may exhibit poor ovarian response. The relative importance of LH supplementation in IVF and other protocols remains a topic of ongoing research and individualized treatment planning, with decisions guided by patient history, ovarian reserve, and prior responses to stimulation.
Cross-references: - hCG - IVF - recombinant LH
In disorders and diagnostic use
LH is routinely measured in the evaluation of pituitary function and suspected gonadal disorders. Abnormally low LH can indicate hypogonadotropic hypogonadism or pituitary disease, whereas elevated or inappropriately high LH with low sex steroids can point to gonadal resistance or certain tumor conditions. In females, the pattern of LH relative to FSH across the cycle is used, in part, to diagnose ovulatory disorders and to assess risks associated with polycystic ovary syndrome (PCOS), where a relative increase in LH secretion is often discussed in relation to androgen excess, though the exact role of the LH/FSH ratio is debated and context-dependent. In puberty, rising LH levels reflect the maturation of the hypothalamic-pituitary-gonadal axis and the onset of reproductive capability. In menopause, LH levels typically rise due to loss of negative feedback from estrogen, serving as one indicator of hormonal aging.
Cross-references: - hypogonadotropic hypogonadism - polycystic ovary syndrome - ovulatory disorders
Controversies and Debates
Within clinical and research communities, several topics concerning LH generation, measurement, and therapeutic use are debated. Some discussions focus on the precise diagnostic value of the LH:FSH ratio in PCOS and its implications for treatment choices. Others examine the efficacy and necessity of LH supplementation in controlled ovarian stimulation for IVF, weighing potential improvements in follicular response against cost and complexity of regimens. There are also ongoing refinements in the interpretation of LH surge timing and its reliability in home ovulation tests, especially given interindividual and cycle-to-cycle variability. These debates center on optimizing fertility outcomes while minimizing risks and unnecessary interventions, rather than ideological positions, and they illustrate how nuanced endocrine signaling is in real-world clinical practice.
Cross-references: - polycystic ovary syndrome - IVF - ovulation