The Polycystic Ovary Syndrome and the Metabolic Syndrome: A Possible Chronobiotic-Cytoprotective Adjuvant Therapy

Abstract

Polycystic ovary syndrome is a highly frequent reproductive-endocrine disorder affecting up to 8–10% of women worldwide at reproductive age. Although its etiology is not fully understood, evidence suggests that insulin resistance, with or without compensatory hyperinsulinemia, and hyperandrogenism are very common features of the polycystic ovary syndrome phenotype. Dysfunctional white adipose tissue has been identified as a major contributing factor for insulin resistance in polycystic ovary syndrome. Environmental (e.g., chronodisruption) and genetic/epigenetic factors may also play relevant roles in syndrome development. Overweight and/or obesity are very common in women with polycystic ovary syndrome, thus suggesting that some polycystic ovary syndrome and metabolic syndrome female phenotypes share common characteristics. Sleep disturbances have been reported to double in women with PCOS and obstructive sleep apnea is a common feature in polycystic ovary syndrome patients. Maturation of the luteinizing hormone-releasing hormone secretion pattern in girls in puberty is closely related to changes in the sleep-wake cycle and could have relevance in the pathogenesis of polycystic ovary syndrome. This review article focuses on two main issues in the polycystic ovary syndrome-metabolic syndrome phenotype development: (a) the impact of androgen excess on white adipose tissue function and (b) the possible efficacy of adjuvant melatonin therapy to improve the chronobiologic profile in polycystic ovary syndrome-metabolic syndrome individuals. Genetic variants in melatonin receptor have been linked to increased risk of developing polycystic ovary syndrome, to impairments in insulin secretion, and to increased fasting glucose levels. Melatonin therapy may protect against several metabolic syndrome comorbidities in polycystic ovary syndrome and could be applied from the initial phases of patients' treatment.

Effects of Melatonin Supplementation on Hormonal, Inflammatory, Genetic, and Oxidative Stress Parameters in Women With Polycystic Ovary Syndrome

“…So, women with PCOS who have high oxidative stress are synthesizing more melatonin, probably in an effort to eliminate extra free radicals (21). High melatonin level in the ovarian follicle fluid is pivotal for ovulation, follicular growth, and quality of oocyte, whereas reduced melatonin level in follicular fluid may be responsible for decreased oocyte quality and anovulation in these women (22). In a recent study, melatonin and myo-inositol co-supplementation significantly improved embryo and oocyte quality in women with PCOS who were candidates for IVF, when compared with myo-inositol alone (23).…”

Investigation of common risk factors between polycystic ovary syndrome and Alzheimer’s disease: a narrative review

“…Studies have shown that higher levels of testosterone in PCOS patients are related to OSA [ 79 ]. This is why sleep disorders in patients with PCOS are twice as common as in ordinary people [ 80 ]. Hyperandrogenism, IR, and low estrogen and progesterone levels with PCOS have all been suggested to cause OSA in PCOS patients [ 81 ].…”

Research progress of endometrial receptivity in patients with polycystic ovary syndrome: a systematic review

“…The main cause of IR in PCOS patients is the inhibition of the insulin signaling molecule transduction pathway due to the phosphorylation of the serine residues of the insulin receptor substrate molecule [ 102 ]. Moreover, alterations in certain genetic material may lead to blockage of insulin secretion and cause IR, such as the MTNR1B gene [ 91 ]. The pathological process of IR in PCOS patients is suggested to be concerned with the disturbance of intestinal flora.…”