Body Composition, Serum Concentrations of Androgens and Insulin Resistance in Different Polycystic Ovary Syndrome Phenotypes

Abstract

Insulin resistance and hyperandrogenemia observed in polycystic ovary syndrome (PCOS) are associated with metabolic disturbances and could be connected with body composition pattern. To date, several studies defining the parameters of body composition using dual energy X-ray absorptiometry (DXA) method in the group of PCOS patients have been published, however, without the analysis in different phenotypes. The aim of the present study was to investigate the relationships between serum androgens concentration, insulin resistance and distribution of fat mass using DXA method in various PCOS phenotypes according to the Rotterdam criteria. We examined 146 women: 34 (38%) had PCOS phenotype A, 20 (23%) phenotype B, 20 (23%) phenotype C and 15 (16%) phenotype D (with mean age of each phenotype 25 years), and 57 control subjects (mean age of 25.5 years). Homeostasis model assessment of insulin resistance (HOMA-IR) was calculated. Serum concentrations of testosterone, androstenedione and dehydroepiandrosterone sulfate (DHEA-S) were assessed and free androgen index (FAI) was calculated. In phenotypes A, B and C, we observed higher FAI in comparison to the control group (all p < 0.01). Serum concentrations of androstenedione and DHEA-S were higher in phenotypes A and C in comparison to the control group (all p < 0.01). However, only in phenotype A we found higher visceral adipose tissue (VAT) mass and android/gynoid ratio (A/G ratio) in comparison to the control group (all p < 0.01). In phenotype A, we observed connection of VAT with FAI (r = 0.58, p < 0.01). Accordingly, A/G ratio was related with FAI in all phenotypes (all p < 0.05). Additionally, in phenotype C, A/G ratio was related to serum concentrations of DHEA-S and androstenedione (r = 0.46, p = 0.03; r = 0.53, p = 0.01, respectively). We also found connections of HOMA-IR with VAT and A/G ratio in all phenotypes (all p < 0.05). Women with phenotype A had higher amount of VAT and A/G ratio in comparison to the control group. Serum concentration of androgens and insulin resistance are connected with VAT and A/G ratio in normoandrogenic and hyperandrogenic PCOS phenotypes.

Comparison of Anti-müllerian Hormone (AMH) and Hormonal Assays for Phenotypic Classification of Polycystic Ovary Syndrome

“…However, in contrast with our results, they did not find a statistically significant difference between phenotype D vs phenotype B and C [31]. Polak's study showed that the mean of FAI in hyperandrogenic phenotypes of PCOS was markedly higher than control group while phenotype D and control groups were similar [32]. In the comparison of PCOS subgroups in terms of FAI, there was a significant increase only in phenotype A compared to the phenotype D [32].…”

Risk of Insulin Resistance and Metabolic Syndrome in Women with Hyperandrogenemia: A Comparison between PCOS Phenotypes and Beyond

“…By showing a similar effect of androgen excess in the group with one Rotterdam criterion only (1RC), we were able to show that metabolic changes not only occur in women with two or more PCOS criteria, but also in women with hyperandrogenemia alone. Some previous studies have described a similar effect with regard to risk of diabetes or the metabolic syndrome [ 7 , 31 ]. However, they did not assess the early effect of developing IR, nor did they take into account the potential PCOS phenotypes using the Rotterdam criteria.…”

“…In our cohort, phenotypes with HA (A-C) had higher average values of BMI and HOMA, while showing lower SHBG and Matsuda values. Previous studies by Polak et al and Gupta et al did not find any significant differences in IR prevalence [ 7 , 28 ]. However, this could be explained by a lower sample size (146 and 150, respectively, compared to 750 women included in our analysis) and their lack of Matsuda index calculation.…”

“…Since the establishment of the Rotterdam consensus in 2003, PCOS has been defined by the presence of at least two out of three criteria: clinical or biochemical hyperandrogenism (HA), oligo- or amenorrhea (OM) and/or polycystic ovarian morphology (PCOM) [ 3 ]. In addition to these three central characteristics of PCOS, many women have several other comorbidities or consecutive diseases, including insulin resistance (IR) [ 4 ] with a high risk for the development of diabetes mellitus, low grade inflammation as well as dyslipidemia and obesity [ 5 , 6 , 7 ].…”

The comparison of the effectiveness and safety of drospirone ethinyl estradiol and ethinyl estradiol cyproterone in the treatment of polycystic ovarian syndrome

“…Clinically, it is characterized by persistent non-ovulation, bio-chemical or clinical manifestations of high androgens, and ovarian polycystic changes, and it often accompanied by obesity and insulin resistance. [ 3 – 4 ] At present, the pathogenesis of PCOS is not completely clear, some studies believe that genetic factors, the abnormalities of hypothyroidism-pituitary-ovary axis regulation, adrenal endocrine mechanism disorders, ovarian local side secretion and self-secretion regulation mechanism imbalance, hypersotrophicemia and insulin resistance, the imbalance between inflammation factors and anti-inflammatory factors may lead to the occurrence of the disease. [ 5 – 6 ]…”