Glycolytic Dysfunction in Granulosa Cells and Its Contribution to Metabolic Dysfunction in Polycystic Ovary Syndrome
June 2025
in “
Drug Design Development and Therapy
”
glycolytic dysfunction granulosa cells polycystic ovary syndrome PCOS glycolysis AMPK mTOR glucose uptake oxidative stress epigenetic changes non-coding RNAs metformin resveratrol mogroside V nicotinamide mononucleotide NMN insulin sensitivity ovarian function AMP-activated protein kinase mechanistic target of rapamycin
This review discusses the role of glycolytic dysfunction in granulosa cells and its contribution to the metabolic and reproductive abnormalities observed in polycystic ovary syndrome (PCOS). It highlights how disrupted glycolysis impairs follicular development and oocyte quality, exacerbating PCOS symptoms. Dysregulated energy-sensing pathways, such as AMPK and mTOR, lead to reduced glucose uptake and increased oxidative stress, worsening the condition. Epigenetic changes and non-coding RNAs also play a role in destabilizing metabolic homeostasis. Therapeutic agents like metformin, resveratrol, mogroside V, and nicotinamide mononucleotide (NMN) show potential in restoring glycolytic balance and improving insulin sensitivity and ovarian function. The review emphasizes the importance of targeting glycolysis for future PCOS therapies.
