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Research Article

Open Vet J. 2026; 16(3): 1885-1892


Cholesterol and testosterone dynamics in a polycystic ovary syndrome animal model

Yudit Oktanella, Amelia Dea Suryadi, Risa Yuliana, Jamilaturrosyidah Jamilaturrosyidah, Andre Giovanni, Nabilla Rizky Mahalita, Anna Listya Poetranto.



Abstract
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Background:
Polycystic Ovary Syndrome (PCOS) is a complex endocrine disorder characterized by hyperandrogenism, elevated Luteinizing Hormone (LH), reduced Follicle Stimulating Hormone (FSH), increased estrogen/estradiol levels, anovulation/oligoovulation, and dyslipidemia, including elevated blood cholesterol levels. Understanding the interplay between hormonal imbalances and metabolic dysregulation in PCOS remains a critical area of research.

Aim:
This study identified the impact of testosterone propionate and estradiol benzoate on cholesterol and testosterone level in a rat model of PCOS.

Methods:
This study employed a testosterone propionate (TP) and oestradiol benzoate (EB) induced female Wistar rat model of PCOS to explore a possible link between cholesterol and testosterone levels in the context of hormonal and metabolic interactions inherent to the syndrome. Six-month-old female Wistar rats (130–150 g) were randomly allocated into three experimental groups: Animals were divided into three groups: NC (corn oil, 100 µL, i.p.), TP (testosterone propionate 100 mg/kg BW, i.p., 12 days), and EB (oestradiol benzoate 2 mg/kg BW, i.p., 2 days).

Results:
Serum cholesterol and testosterone levels were measured and compared across groups. Induction with TP and EB did not significantly alter cholesterol levels in the PCOS model compared to the NC group (P ≥ 0.05). However, while testosterone levels in the TP group showed no significant difference from the control (P ≥ 0.05), the EB group demonstrated a statistically significant increase in testosterone levels relative to the control (P ≤ 0.05).

Conclusion:
The findings indicate that oestradiol benzoate, but not testosterone propionate, significantly elevates testosterone levels in this PCOS model, without a corresponding impact on cholesterol levels. These results underscore the differential effects of hormonal induction on androgen production and lipid metabolism, providing insights into the complex pathophysiology of PCOS. Further research is warranted to explore the mechanisms underlying these hormonal and metabolic interactions.

Key words: PCOS; Testosterone; Estradiol benzoate; Endocrine disorder; Cholesterol







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