Potential effects of adropin on systemic metabolic and hormonal abnormalities in polycystic ovary syndrome
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Updated: Nov 16, 2025

Author Spotlight: Investigating the Mechanisms and Inducing Models of Polycystic Ovary Syndrome
Published on: July 5, 2024
Zhenhong Ye1, Chunmei Zhang1, Yue Zhao2
1Center for Reproductive Medicine, Department of Obstetrics and Gynecology, Peking University Third Hospital Beijing, China; National Clinical Research Center for Obstetrics and Gynecology (Peking University Third Hospital) Beijing, China; Key Laboratory of Assisted Reproduction, Ministry of Education (Peking University) Beijing, China; Beijing Key Laboratory of Reproductive Endocrinology and Assisted Reproductive Technology Beijing, China.
Research Question:
The study aimed to explore the effects of adropin on hormone concentrations and glucolipid and amino acid metabolism in patients with polycystic ovary syndrome (PCOS).
Design:
A total of 220 PCOS patients and 67 controls were recruited and basal state plasma was collected for adropin measurement. Follicular fluids from 50 PCOS patients and 30 controls were also collected for adropin analysis.
Results:
Plasma and follicular fluid adropin concentrations were lower in PCOS patients than controls (P < 0.001; P = 0.017). Adropin concentrations were negatively correlated with body mass index (BMI), free androgen index, Homeostatic Model Assessment of Insulin Resistance (HOMA-IR), androstenedione and triglycerides, and positively correlated with sex hormone-binding globulin (SHBG) and high-density lipoprotein (HDL) (all P < 0.05). PCOS patients who were either obese or glucose intolerant had lower adropin concentrations (P < 0.001). Follicular fluid adropin concentrations were negatively correlated with HOMA-IR, isoleucine and valine in the PCOS group (all P < 0.05). After adjusting for age, BMI, HOMA-IR and HDL, SHBG still significantly impacted the concentration of plasma adropin (P = 0.022). After adjusting for age and BMI, the odds of subjects with reduced adropin concentrations having PCOS still remained significant (P = 0.045). The association between plasma adropin and PCOS disappeared following SHBG adjustment.
Conclusions:
The concentrations of adropin in plasma and follicular fluid were lower in PCOS patients, which might affect the development of insulin resistance. The association between adropin concentrations and hyperandrogenaemia in PCOS might be mediated through SHBG. The decreased adropin concentrations are associated with abnormal branched-chain amino acid metabolism in PCOS.
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