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Follicle-stimulating hormone (FSH) is a gonadotropin, a glycoprotein polypeptide hormone. [1] FSH is synthesized and secreted by the gonadotropic cells of the anterior pituitary gland [ 2 ] and regulates the development, growth, pubertal maturation , and reproductive processes of the body.
Hypergonadotropic hypogonadism (HH), also known as primary or peripheral/gonadal hypogonadism or primary gonadal failure, is a condition which is characterized by hypogonadism which is due to an impaired response of the gonads to the gonadotropins, follicle-stimulating hormone (FSH) and luteinizing hormone (LH), and in turn a lack of sex steroid production. [1]
Gonadotropins are glycoprotein hormones secreted by gonadotropic cells of the anterior pituitary of vertebrates. [1] [2] [3] This family includes the mammalian hormones follicle-stimulating hormone (FSH) and luteinizing hormone (LH), the placental/chorionic gonadotropins, human chorionic gonadotropin (hCG) and equine chorionic gonadotropin (eCG), [3] as well as at least two forms of fish ...
Clinical presentations of CHH involve an absence of puberty by 18 years of age, poorly developed secondary sexual characteristics, or infertility. [12] In men with CHH, serum levels of inhibin B are typically very low as inhibin B is a marker of Sertoli cell number. [4] For females, CHH is most commonly revealed by primary amenorrhea.
In the male, the FSH receptor has been identified on the Sertoli cells that are critical for spermatogenesis. [12] The FSHR is expressed during the luteal phase in the secretory endometrium of the uterus. [13] FSH receptor is selectively expressed on the surface of the blood vessels of a wide range of carcinogenic tumors. [14]
Gonadorelin is used as a diagnostic agent to assess pituitary gland function. [1] It is also used in the treatment of primary hypothalamic amenorrhea, hypogonadotropic hypogonadism (e.g., Kallmann syndrome), delayed puberty, cryptorchidism, and infertility. [7] [8] [1] Unlike other GnRH analogues, it is not used to suppress sex hormone ...
LH is released from the pituitary gland along with FSH in response to GnRH release into the hypophyseal portal system. [4] Pulsatile GnRH release causes pulsatile LH and FSH release to occur, which modulates and maintains appropriate levels of bioavailable gonadal hormone—testosterone in males and estradiol in females—subject to the requirements of a superior feedback loop. [3]
Sertoli cells are required for male sexual development. Sertoli cell proliferation and differentiation is mainly activated by FGF9, with which they also form a feedforward loop. [4] [5] It has been suggested that Sertoli cells may derive from the fetal mesonephros. [6] After puberty, Sertoli cells begin to elongate.