Abstract
Subfertility is one of the features of polycystic ovary syndrome (PCOS) that has a significant impact on a couple’s life and is negatively associated with features like depression and anxiety. The pathology involved here is complex with multiple factors involved at the level of hypothalamus, pituitary, ovary, and endometrium. Increase GnRH pulses from hypothalamus cause increase Leutinizing hormone (LH) from the anterior pituitary, which in turn drives excessive androgen from the theca cells of the ovaries. Hirsutism, acne, and polycystic appearance of ovaries are considered to be the clinical manifestation of high androgen levels. Normally in females, high androgens are converted into estradiol by the enzyme aromatase, which in PCOS is either deficient or defective. Thus, relatively low levels of FSH and estradiol results in premature arrest of follicles maturation and ovulation abnormalities. Obesity and insulin resistance also has a significant part to play in this regard. Obesity increases the insulin resistance and hyperinsulinemia in turn decreases the sex hormone binding globulin (SHBG) levels, further increasing the free testosterone levels. This hyperandrogenism is mainly functional hyperandrogenism and these biochemical abnormalities contribute to the development of polycystic ovarian morphology and ovulation dysregulation and subfertility.
Original language | English |
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Title of host publication | Polycystic Ovary Syndrome |
Subtitle of host publication | Basic Science to Clinical Advances across the Lifespan |
Publisher | Elsevier |
Pages | 51-55 |
Number of pages | 5 |
ISBN (Electronic) | 9780323879323 |
ISBN (Print) | 9780323879330 |
DOIs | |
Publication status | Published - 1 Jan 2023 |
Keywords
- androgens
- anovulation
- follicle stimulating hormone (FSH)
- hyperinsulinemia
- luteinizing hormone (LH)
- obesity
- polycystic ovarian syndrome (PCOS)
- sex hormone–binding globulin (SHBG)
- subfertility