Yudit Oktanella, Muhammad Reza Fahlevi, Handayu Untari, Viski Fitri Hendrawan, Nabilla Rizky Mahalita, Jamilaturrosyidah Jamilaturrosyidah, Anna Lystia Poetranto
Background: Polycystic ovary syndrome (PCOS) is a prevalent endocrine disorder that can lead to metabolic and reproductive complications, including liver dysfunction. Despite its widespread occurrence, the mechanisms linking PCOS to hepatic impairment remain unclear, necessitating reliable animal models for further investigation. Aim: This study evaluates the impact of testosterone propionate and estradiol benzoate on liver function in a rat model of PCOS. Methods: A completely randomized design was implemented using 18 female Wistar rats divided into three groups. The control group received 0.9% NaCl orally, while group 1 received testosterone propionate (100 mg/kg body weight, intraperitoneally), and Group 2 received estradiol benzoate (2 mg/kg BW, intraperitoneally). After 28 days, serum glutamic-pyruvic transaminase (SGPT) and glutamic oxaloacetic transaminase (SGOT) levels were measured, and liver histopathology was assessed for hepatocyte necrosis. Results: One-way ANOVA showed a statistically significant difference in SGOT levels among groups (p < 0.05), with the lowest mean observed in the estradiol group (G2). However, the SGPT levels and histopathological scoring of hepatocyte necrosis did not significantly differ between the groups. All groups exhibited mild to moderate necrosis, which may have been influenced by environmental factors such as ammonia exposure. Conclusion: Acute induction of PCOS using testosterone propionate and estradiol benzoate resulted in modest hepatocellular changes, with only SGOT levels showing a significant group difference. These findings suggest that the hepatic response is limited under the tested conditions. Future studies should consider longer exposure durations, combined metabolic stressors, and environmental controls to better simulate PCOS-associated liver dysfunction and to develop more robust animal models for therapeutic evaluation. © 2025, Faculty of Veterinary Medicine, University of Tripoli. All rights reserved.
Department of Veterinary Reproduction, Faculty of Veterinary Medicine, Universitas Brawijaya, Malang, Indonesia; Faculty of Veterinary Medicine, Universitas Brawijaya, Malang, Indonesia; Department of Pathology, Faculty of Veterinary Medicine, Universitas Brawijaya, Malang, Indonesia; National Research and Innovation Agency (BRIN), Bogor, Indonesia
