"Mechanistic Insights into Androgen Excess and Insulin Resistance in PCOS: Preclinical Evidence and Alternative Models for Translational Research"

 Introduction:

 Polycystic ovary syndrome (PCOS) is a complex endocrine, metabolic, and reproductive disorder affecting 6–20% of reproductive-age women worldwide. A hallmark of PCOS is androgen excess, which plays a crucial role in its pathophysiology, along with insulin resistance (IR). These factors contribute to reproductive dysfunction, metabolic abnormalities, and long-term health risks such as type 2 diabetes and cardiovascular diseases. Despite extensive research, the exact mechanisms underlying PCOS remain unclear, necessitating further exploration of androgen metabolism, insulin signaling, and alternative therapeutic strategies.


Methods:

This synthesizes findings from preclinical studies (in vivo and in vitro models) and computational approaches to elucidate the role of androgens and insulin resistance in PCOS.

·        Animal Models: Insights from rodent models of hyperandrogenism and insulin resistance (e.g., postnatal androgen exposure, letrozole-induced PCOS models).

·        Molecular Pathways: Analysis of IRS1/AKT, AMPK, and NF-κB signaling in androgen-mediated metabolic dysfunction.

·        Cell-Based Studies: Examination of adipocyte and theca cell cultures to study androgen biosynthesis and metabolic disturbances.

·        In Silico Studies: Molecular docking to explore interactions between androgen-regulating enzymes and therapeutic compounds.





 C   Conclusion:

Preclinical studies provide compelling evidence that androgen excess and insulin resistance synergistically drive PCOS pathogenesis. Targeting AR signaling, mitochondrial dysfunction, and AMPK pathways may offer new therapeutic avenues. Future research should focus on alternative models that reduce reliance on animal testing, such as organ-on-chip systems, computational modeling, and human-derived cell cultures, to advance PCOS research while aligning with ethical research practices.

Keywords: PCOS, Androgen Excess, Insulin Resistance, AMPK Oxidative Stress, Metabolic Dysfunction.


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