The study and all experimental procedures were approved by the Ethics Committee of Peking University Third Hospital according to the Council for International Organizations of Medical Sciences. All participants were recruited from the Reproductive Medical Center at Peking University Third Hospital between September 2015 and December 2016. For cohort 1, we recruited 50 individuals with PCOS and 43 controls of Chinese ancestry. Written informed consent was obtained from all participants.
Women with PCOS were diagnosed according to the 2003 Rotterdam criteria, which require the presence of at least two of the following: (1) oligo-ovulation and/or anovulation; (2) clinical and/or biochemical signs of hyperandrogenism; and (3) polycystic ovaries. Diagnoses of PCOS were made after the exclusion of other etiologies for hyperandrogenemia or ovulatory dysfunction (Cushing syndrome, 21-hydroxylase deficiency, thyroid disease, androgen-secreting tumors, congenital adrenal hyperplasia and hyperprolactinemia). All individuals with PCOS were first-visit patients and had not received PCOS-related treatment. The control subjects were from the general community and had regular menstrual cycles, normal ovarian morphology and normal levels of hormones. Women who were breastfeeding or pregnant within the past year or who took medication within the past 3months were excluded from the study.
Height, body weight, waist circumference and hip circumference were measured, and the body mass index (kgm−2) and waist-to-hip ratio were calculated. Peripheral blood samples were collected from all subjects during days 2–4 of spontaneous cycles after an overnight fast.
Levels of serum FSH, luteinizing hormone and SHBG were tested by radioimmunoassays. The levels of estradiol, testosterone, androstenedione and DHEA sulfate were measured using liquid chromatography–mass spectrometry (Sciex Triple Quad 6500+). The free androgen index was defined as (testosterone (nmoll−1)×100)/SHBG (nmoll−1). The levels of fasting serum glucose, serum insulin, triglycerides, total cholesterol, high-density lipoprotein cholesterol and low-density lipoprotein cholesterol were measured using an autoanalyzer (Beckman Coulter AU5800). The insulin resistance index (HOMA-IR) was calculated using homeostasis model assessment methods, defined as fasting insulin (mIUl−1)×fasting glucose (mmoll−1)/22.5.
Women with PCOS were diagnosed according to the 2003 Rotterdam criteria, which require the presence of at least two of the following: (1) oligo-ovulation and/or anovulation; (2) clinical and/or biochemical signs of hyperandrogenism; and (3) polycystic ovaries. Diagnoses of PCOS were made after the exclusion of other etiologies for hyperandrogenemia or ovulatory dysfunction (Cushing syndrome, 21-hydroxylase deficiency, thyroid disease, androgen-secreting tumors, congenital adrenal hyperplasia and hyperprolactinemia). All individuals with PCOS were first-visit patients and had not received PCOS-related treatment. The control subjects were from the general community and had regular menstrual cycles, normal ovarian morphology and normal levels of hormones. Women who were breastfeeding or pregnant within the past year or who took medication within the past 3months were excluded from the study.
Height, body weight, waist circumference and hip circumference were measured, and the body mass index (kgm−2) and waist-to-hip ratio were calculated. Peripheral blood samples were collected from all subjects during days 2–4 of spontaneous cycles after an overnight fast.
Levels of serum FSH, luteinizing hormone and SHBG were tested by radioimmunoassays. The levels of estradiol, testosterone, androstenedione and DHEA sulfate were measured using liquid chromatography–mass spectrometry (Sciex Triple Quad 6500+). The free androgen index was defined as (testosterone (nmoll−1)×100)/SHBG (nmoll−1). The levels of fasting serum glucose, serum insulin, triglycerides, total cholesterol, high-density lipoprotein cholesterol and low-density lipoprotein cholesterol were measured using an autoanalyzer (Beckman Coulter AU5800). The insulin resistance index (HOMA-IR) was calculated using homeostasis model assessment methods, defined as fasting insulin (mIUl−1)×fasting glucose (mmoll−1)/22.5.
