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Updated: Mar 24, 2026

Evaluation of Hepatic Glucose Production in a Polycystic Ovary Syndrome Mouse Model
Published on: March 5, 2022
A possible connection between tumor necrosis factor alpha and adropin levels in polycystic ovary syndrome
1Department of Biochemistry and Clinical Biochemistry, Dokuz Eylul University Faculty of Medicine, 35340, Inciralti, Izmir, Turkey.
Context:
Adropin is a peptide hormone implicated in the regulation of insulin sensitivity and energy homeostasis. Polycystic ovary syndrome (PCOS) is a metabolic and reproductive disease associated with insulin resistance. It has been demonstrated that various inflammatory markers increased in PCOS including TNF-α. TNF-α regulates the secretion of certain peptides which play a crucial role in glucose and lipid homeostasis. There is also some evidence of a link between TNF-α and adropin.
Objective:
To ascertain whether there is an association between circulating adropin levels and TNF-α in PCOS.
Patients And Design:
152 women with PCOS and 152 age- and body mass index-matched controls without PCOS were recruited for this cross-sectional study.
Main Outcome Measures:
Adropin and TNF-α levels were measured using ELISA.
Results:
Adropin levels were lower in the PCOS group compared with the control group (7.43 ± 0.79 vs. 9.42 ± 0.76 ng/ml, P < 0.001), whereas TNF-α levels were higher (49.93 ± 3.39 vs. 35.83 ± 2.47 pg/ml, P < 0.001). A strongly negative correlation was found between circulating adropin levels and TNF-α levels in women with PCOS (r = -0.407, P < 0.001). Binary logistic regression analysis revealed that decreased adropin levels were significantly associated with high odds of having PCOS, although, after adjustment for TNF-α, this link vanished. Additionally, multiple linear regression analysis showed that HOMA-IR and TFN-α independently predicted adropin levels.
Conclusions:
Serum adropin levels are significantly decreased in PCOS and are inversely associated with TNF-α. Further dissection of the nature of this association can open new therapeutic options for metabolic diseases.
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