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 atreproductive age. Although its etiology is not fully understood, evidence suggests that insulin resistance, with or withoutcompensatory 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 ovarysyndrome. Environmental (e.g., chronodisruption) and genetic/epigenetic factors may also play relevant roles in syndromedevelopment. Overweight and/or obesity are very common in women with polycystic ovary syndrome, thus suggesting thatsome polycystic ovary syndrome and metabolic syndrome female phenotypes share common characteristics. Sleep disturbanceshave been reported to double in women with PCOS and obstructive sleep apnea is a common feature in polycystic ovarysyndrome patients. Maturation of the luteinizing hormone-releasing hormone secretion pattern in girls in puberty is closelyrelated to changes in the sleep-wake cycle and could have relevance in the pathogenesis of polycystic ovary syndrome. Thisreview article focuses on two main issues in the polycystic ovary syndrome-metabolic syndrome phenotype development: (a) theimpact of androgen excess on white adipose tissue function and (b) the possible efficacy of adjuvant melatonin therapy toimprove the chronobiologic profile in polycystic ovary syndrome-metabolic syndrome individuals. Genetic variants in melatoninreceptor have been linked to increased risk of developing polycystic ovary syndrome, to impairments in insulin secretion, and toincreased fasting glucose levels. Melatonin therapy may protect against several metabolic syndrome comorbidities in polycysticovary syndrome and could be applied from the initial phases of patients? treatment.