Changes in Glycosylation of Pituitary Gonadotropins in Polycystic Ovary Syndrome SciDoc Publishers | Open Access | Science Journals | Media Partners

The clinical features of polycystic ovary syndrome (PCOS) are comprised of obesity, hirsutism and amenorrhea, with the presence of pearly-appearing enlarged ovaries with multiple follicular cysts [1-2]. Both the initial description of this syndrome and the diagnosis have continuously evolved; therefore, the pathogenesis is a source of contradictions and theories [3-4]. These changes are due to the incorporation of continuous improvements in the methods and techniques of hormonal measurements as well as imaging methods, particularly vaginal ultrasound [5-7]. There is no consistent hormonal profile because the measurement of circulating hormones with the current analytical methods yields varying results, which in many cases are difficult to interpret [8-10]. PCOS has multiple endocrine and metabolic implications that have created a multicausal approach in its pathophysiology. Among the multiple causes is the reported central nervous system (CNS) involvement, with the control regulation center of gonadotropin-releasing hormone (GnRH), the pituitary with the gonadotrope and the portal system connected to the hypothalamus, the participation of the insulin resistance complex and hyperinsulinemia with consequent hyperandrogenism status, degree of obesity, the genetic component along the endocrine system and the involvement of adrenal glands with late-onset congenital adrenal hyperplasia [11-14]. Because we are dealing with gonadotropins in this study, it is important to note the regulatory links between the CNS and the ovaries with their estrogen hormone production [15,16]. Gonadotropins are synthesized and secreted by specialized cells called gonadotropes, which are found in the anterior pituitary and synthesize both FSH and LH [17,18]. It is known that the molecular forms of gonadotropins can vary in relation to hormonal status that predominates at each stage of life and typically correspond to changes in estrogen levels during physiological conditions such as puberty and the ovarian cycle, indicating that the FSH pleomorphism is a hormonally regulated phenomenon [19]. The clinical manifestation of this is that circulating FSH and LH have greater biological activity when they have incorporated a smaller amount of sialic acid. On the other hand, they have a longer half-life when they have incorporated a larger amount of sialic acid due to the protection offered to the molecule and thus have a prolonged biological effect. Thus, isoforms with less sialization are more potent than strongly sialized forms to induce proliferation of granulose cells and to prevent