EDITORIAL February 01, 2020 February 01, 2020

Polycystic ovary syndrome: new insights on the puzzle of adiposity, chronic low-grade inflammation and metabolic disturbances

DOI: 10.20945/2359-3997000000205

Polycystic ovary syndrome (PCOS) is a frequent and complex condition affecting women of reproductive age and is characterized by hyperandrogenism, irregular menstrual cycles and polycystic ovarian morphology (PCOM). Women with PCOS also present higher prevalence of obesity, metabolic disturbances and functional perturbations in adipose tissue. Emerging evidence suggests that hyperandrogenism may induce adipocytes proliferation, as observed in women with PCOS. Also, higher percentage of body fat mass and androgen excess have been associated with insulin resistance ( ). Expansion of adipose tissue has been linked to altered secretion of adipokines, inflammation and apoptosis. The hypertrophy of adipocytes and androgen excess in PCOS lead to chronic low-grade inflammation related to compression phenomena in the stromal vessels, local hypoperfusion and disturbed cytokines production. These derangements on the adipose tissue function and secretion may influence the pathophysiology of PCOS through their impact on metabolism and on sex steroid secretion ( ).

In this issue of AE&M, Cardoso and cols. ( ) report the associations between adiposity, metabolic traits and adipose tissue-secreted products in a sample of women with PCOS compared to controls. The subjects were stratified according to body fat percentage (BFP) classes and both PCOS and controls were similar regarding age, body mass index (BMI), waist-to-hip ratio, body fat and lipid profile in each BFP class. In turn, considering the same body fat class, insulin-resistance markers (insulin and HOMA-IR) as well as testosterone levels were higher in PCOS compared to controls. Leptin levels were similarly higher and adiponectin levels were lower in both PCOS and control subgroups presenting greater adiposity. In contrast, in these subjects with greater body fat, inflammation markers – TNFα and IL6 levels were higher in PCOS compared to controls. The outcomes of this study, analyzing adipokine levels associated to body fat instead of BMI, expand previous published data about leptin circulating levels in PCOS and controls that indicated a direct relationship between leptin and the amount of body fat, being significantly increased in overweight or obese subgroups, in the presence of PCOS or not ( , ). Conversely, current data are not yet conclusive in relation to adiponectin serum levels, as also cited by Cardoso and cols., and other studies have found lower adiponectin levels in women with PCOS compared with controls ( ). The disagreement among studies may be related to distinct factors, such as ethnicity or to differences in the methods of adiponectin determination. Recently, the measurement of high molecular weight-active adiponectin forms instead of total adiponectin has shown to increase the accuracy of assessments of the relationship between adiponectin and insulin resistance in PCOS ( , ). Interestingly, the results of the Cardoso et al study also reinforce the notion that higher/dysfunctional fat mass in PCOS may release inflammatory mediators, such as TNF and IL6, contributing to pathophysiological mechanisms related to the development of metabolic and reproductive dysfunctions of the syndrome ( , ).

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