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Published in Asim Kurjak, Ultrasound and Infertility, 2020
Joseph G. Schenker, Aby Lewin, Menashe Ben-David
A variety of treatment schedules for gonadotropin administration for induction of ovulation have been devised. Nearly all of those schedules are based on the fact that treatment with gonadotropin preparations results specifically in follicular growth and maturation. The “variable technique” has been used more commonly; the daily dosage and duration of therapy depend on individual response. Gonadotropin preparations are very active agents for stimulating the ovary to ovulate, and with adequate therapy ovulation is achieved in 80 to 90% of the patients, although pregnancy can be expected in only 40 to 60%. The conception rate depends on the selection of patients, dose, regimen, and number of treatment cycles. Gonadotropin therapy can be applied in combination with different agents like clomiphene, Gn-RH, dexamethasone, and parlodel.
Biological Responses in Context
Published in Arthur T. Johnson, Biology for Engineers, 2019
Probably the most familiar monthly cycle is the menstrual cycle in human females and several other primates (Campbell et al., 1999). This cycle begins with the thickening of the lining of the uterus, called the endometriumFigure 6.21.6, and development of a rich blood supply in preparation for possible implantation of an embryo. In response to gonadotrophin-releasing hormone (GnRH) secreted by the hypothalamus, the pituitary gland secretes small amounts of follicle-stimulating hormone (FSH) and luteinizing hormone (LH). The FSH stimulates several ovarian follicles to grow and the enclosed eggs to enlarge. These follicles secrete estrogens. Through a complex feedback loop, the pituitary gland is then stimulated to release a large amount of LH and FSH, causing final maturation of one of the follicles, and the egg is released during ovulation.
EMA-approved biosimilars
Published in Sarfaraz K. Niazi, Biosimilars and Interchangeable Biologics, 2016
Follicle-stimulating hormone (FSH) is a gonadotropic hormone produced by the anterior lobe of the mammalian pituitary gland. It is indispensable for normal female and male gamete growth and maturation, and normal gonadal steroid production. Deficient endogenous production of FSH is a known cause of infertility and administration of exogenous gonadotropins is used to treat this condition. Naturally derived FSH, manufactured from the urine of postmenopausal women, has been available for over 30 years. The availability of recombinant DNA technology allows the manufacture of FSH independently of the collection of large volumes of urine and provides a highly pure product devoid of infectious or pharmacological contaminants such as luteinizing hormone (LH), proteinaceous, or potentially allergenic materials.
Hyperlipidemia and male infertility
Published in Egyptian Journal of Basic and Applied Sciences, 2021
Zainab Bubakr Hamad Zubi, Hamad Abdulsalam Hamad Alfarisi
Gonadotropin releasing hormone (GnRH) from the hypothalamus, gonadotropins; follicle-stimulating hormone (FSH) and luteinizing hormone (LH) from the anterior pituitary gland and testosterone and inhibin from the testes are the group of hormones that regulate the spermatogenesis process [20]. The main target of FSH is Sertoli cells. Through production of several mediators, FSH is essential for development of germ cells, movement of sperm from testis to epididymis, and for control of pH of seminal fluid. Leydig cells are the main target of LH which stimulate testosterone production [21]. (Figure 1) illustrates the histology of testis with the site and stages of spermatogenesis.
How the quest to improve sheep reproduction provided insight into oocyte control of follicular development
Published in Journal of the Royal Society of New Zealand, 2018
Ovarian follicular growth and ovulation is controlled by complex communication among the hypothalamus, pituitary, ovary and uterus (Figure 2). The hypothalamus secretes gonadotrophin releasing hormone (GnRH), which acts on the pituitary to cause synthesis and release of the gonadotrophins, follicle stimulating hormone (FSH) and luteinising hormone (LH) (Clarke & Arbabi 2016). In turn, FSH and LH act on cells in the ovarian follicle to support its growth and maturation (Webb & Campbell 2007). Initially, FSH acts on granulosa cells to stimulate proliferation and differentiation. LH stimulates production of androstenedione from the theca that then is used as a substrate by granulosa cells to produce oestradiol. As the follicle grows, increased amounts of inhibin are also produced by the granulosa cells and, together with oestradiol, these feedback to the pituitary to inhibit FSH synthesis and release (Webb & Campbell 2007). Oestradiol, as well as progesterone produced by the corpus luteum, also inhibit GnRH release from the hypothalamus, suppressing the release of the gonadotrophins (Goodman et al. 2002). However, as the follicle continues to grow, the granulosa cells mature and they begin to express LH receptors (LHR). FSH concentrations fall during selection of the follicles that will go on to ovulation. Follicles that are mature enough to express LHR on the granulosa cells are able to survive through the additional support of LH, as FSH concentrations are suppressed. Less mature gonadotrophin dependent follicles, that have yet to express LHR on the granulosa cells, die in this environment. The mature follicles continue to grow and synthesise increasing levels of oestradiol (Webb & Campbell 2007). During the follicular phase, following the regression of the corpus luteum triggered by release of prostaglandin F2α from the uterus (Niswender et al. 2000), oestradiol reaches a critical threshold. At this stage, oestradiol actually switches from negative to positive feedback, causing the release of the preovulatory gonadotrophin surge (Caraty et al. 1995), and ovulation of the mature follicle(s) (usually one or two in sheep).