Luteinizing hormone and human chorionic gonadotropin: distinguishing unique physiologic roles

Figures & data

Figure 1. Relative expression of luteinizing hormone (LH) and human chorionic gonadotropin (hCG) during the stages of life in females (A) and males (B). Note that patterns of LH and hCG expression will vary substantially from person to person. This figure is a representation of which molecule is predominant at the different stages of life. It is not an exact measurement.

Table 1. Phenotypes in knockout and transgenic mice.

Model	Gender	Reproductive phenotype
Disrupted pituitary glycoprotein hormone α-subunit [56]	Female	Prepubertal external genitalia, underdeveloped ovaries and uterus, limited follicle development, absence of ovulation, failure of vaginal orifice opening, infertility
	Male	Prepubertal external genitalia, reduced testes size, impaired spermatogenesis, testosterone deficiency, infertility
LH receptor null [57,58]	Female	Underdeveloped genitalia, ambiguous vaginal opening, arrested follicular growth, decreased estradiol and progesterone levels, infertility
	Male	Underdeveloped genitalia, abdominal testes, micropenis, Leydig cell hypotrophy, disarray of seminiferous tubules, spermatogenic arrest, modestly elevated estradiol levels, infertility
LH β-subunit null [59]	Female	Hypogonadism, decreased serum estradiol and progesterone levels, defects in folliculogenesis, gene expression abnormalities, uterine hypoplasia, infertility
	Male	Decreased testicular size, Leydig cell hypoplasia, gene expression abnormalities, reduced testosterone levels, impaired spermatogenesis, infertility
hCG α-subunit overexpression [60]	Female and male	Normal and fertile*
hCG β-subunit overexpression [60–62]	Female	Precocious puberty, enhanced ovarian steroidogenesis, abnormal uterine structure, hyperprolactinemia, infertility†
	Male	Mild hypogonadism, fertile† Infertility*
hCG α- and β-subunit overexpression [60,61]	Female	Elevated levels of serum estradiol, hemorrhagic and cystic ovaries, thecal layer enlargement, stromal cell proliferation, infertility*, tumorigenesis*
	Male	Increased testicular androgen production, focal Leydig cell hypertrophy, progressive seminiferous tubule degeneration, urethral obstruction, infertility† Leydig cell hyperplasia, very high serum testosterone levels, reduced testis size, enlarged seminal vesicles, infertility*

LH, luteinizing hormone; hCG, human chorionic gonadotropin.

*Transgene expression was driven by the ubiquitin promoter.

†Mice expressing high levels of hCG, with transgene expression driven by the metallothionein 1 promoter.

Table 2. Phenotypes associated with mutations in human LHB, CGB and LHCGR genes*.

Gene and type of mutation	Sex	Phenotype	Effect on fertility
LHB
Inactivating	Women	Oligomenorrhea, secondary amenorrhea	Infertile
	Men	Hypogonadism, Leydig cell hypoplasia, testosterone deficiency, azoospermia	Infertile
Polymorphisms	Women	Endometriosis, hyperprolactinemia, luteal insufficiency, menstrual disorders, PCOS, premature ovarian failure	Reduced fertility
	Men	Increased prostate cancer risk	Unknown
CGB
Polymorphism	Women	Recurrent miscarriage	Reduced fertility
LHCGR
Activating	Men	Familial male-limited gonadotropin-independent precocious puberty Leydig cell adenoma	Not affected Reduced fertility
Inactivating	Women	Oligomenorrhea/amenorrhea, empty follicle syndrome	Infertile
	Men	Leydig cell hypoplasia	Infertile
Polymorphism	Women and men	Risk factor for certain cancers	Unknown

LHB, luteinizing hormone β-polypeptide; CGB, chorionic gonadotropin β-polypeptide; LHCGR, luteinizing hormone/choriogondotropin receptor; PCOS, polycystic ovary syndrome.

*Sources: references [63–81].

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