Abstract

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 (CRD) was implemented using 24 female Wistar rats, divided into three groups. The control group received 0.9% NaCl orally, while Group 1 was induced with testosterone propionate (100 mg/kg BW, intraperitoneally), and Group 2 received estradiol benzoate (2 mg/kg BW, intraperitoneally). After 28 days, serum glutamic-pyruvic transaminase (SGPT) and serum glutamic-oxaloacetic transaminase (SGOT) levels were measured, and liver histopathology was assessed for hepatocyte necrosis.
Results: There were no statistically significant differences (p≤0.05) in SGPT and SGOT levels or liver histopathology among the groups.
Conclusion: The administered doses of testosterone propionate and estradiol benzoate did not induce significant liver dysfunction or alter transaminase levels in this rat PCOS model. These findings highlight the challenge of replicating PCOS-related hepatic complications in animal models. Further research is necessary to refine induction protocols and dosing strategies to develop a more representative model for studying PCOS-associated liver dysfunction and potential therapeutic interventions.

Key words: Animal Model; Liver; Polycystic Ovary Syndrome; SGPT; SGOT