Abstract and Introduction
Objective: Polycystic ovary syndrome (PCOS) is associated with an increased prevalence of dysglycaemia, which includes impaired glucose tolerance and type 2 diabetes mellitus (T2DM). Patients with PCOS demonstrate abnormal patterns of steroid hormones. Here, we analyse the correlation between glucose metabolism and serum steroid hormones in PCOS.
Design: Observational double-centre study.
Patients: 914 patients with PCOS.
Measurements: We assessed the glucose metabolism status of all patients according to the 1999 WHO criteria. Serum steroid hormones were measured by liquid chromatography-tandem mass spectrometry.
Results: The median age of the patients was 26 years (interquartile range: 21–30), and 40.6% (371/914) had abnormal glucose metabolism: 29.3% (268/914) had prediabetes, and 11.3% (103/914) had T2DM. Correlation analysis not adjusting for confounding factors revealed that serum aldosterone, androstenedione, oestrone, pregnenolone and the free androgen index were positively correlated, while progesterone was negatively correlated with the risk of abnormal glucose metabolism. After adjusting for age, body mass index and fasting insulin levels in the logistic regression model, only aldosterone (P = .013), androstenedione (P = .046) and oestrone (P = .014; in quartiles) were correlated with the risk of abnormal glucose metabolism.
Conclusions: This study indicates a high prevalence of prediabetes and T2DM in patients with PCOS. Furthermore, there were positive correlations of serum aldosterone, androstenedione and oestrone with the risk of abnormal glucose metabolism after adjusting for confounding factors.
Polycystic ovary syndrome (PCOS), featuring hyperandrogenism, ovulation disorders and ovarian polycystic changes, most commonly occurs in women of childbearing age and is one of the major aetiologies for hyperandrogenism and infertility in women.[1,2] Moreover, PCOS contributes to metabolic disorders, such as obesity, insulin resistance and hyperglycaemia. In the Danish national registration study, patients with PCOS had a four times higher risk of type 2 diabetes mellitus (T2DM) than normal controls, and the age at diagnosis was younger. A large population-based study in northern California also found that patients with PCOS were more likely to develop diabetes. These findings were consistent with those of a meta-analysis.
However, it remains controversial whether PCOS has an effect on glucose metabolism, irrespective of traditional influencing factors such as age and body mass index (BMI).[7–9] Recently, an Australian longitudinal population-based cohort study showed that in addition to obese women with PCOS, lean women with PCOS also had a higher relative risk of T2DM. Furthermore, after adjusting for BMI, education, area of residence and family history, the T2DM risk had a 3.23-fold increase in women with PCOS compared with those without PCOS. Thus, the heterogeneity of clinical manifestations and the complex mechanism involved in the onset of hyperglycaemia in patients with PCOS merits further exploration.
Patients with PCOS often have abnormal levels of serum steroid hormones, and hyperandrogenism is one of its main characteristics. High androgen levels in these patients may worsen the function of islet beta cells and aggravate insulin resistance through multiple pathways,[2,11,12] thus leading to impaired glucose metabolism. In addition to testosterone, androstenedione and dehydroepiandrosterone sulphate (DHEAS), other steroid hormones, such as aldosterone and cortisol, have been found to be increased in these patients.[13,14] Therefore, further evaluation is required to determine whether these steroid hormones have some relationship with the increased risk of abnormal glucose metabolism in PCOS.
Here, we illustrate steroid hormone profiles in a large-sample, double-centred study in China using liquid chromatography-tandem mass spectrometry (LC-MS/MS) and analyse the association between glucose metabolism and serum steroid hormones in patients with PCOS.
Clin Endocrinol. 2020;92(4):350-357. © 2020 Blackwell Publishing