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Background <p>Polycystic ovary syndrome (PCOS) is a multifactorial disorder associated with insulin resistance, hyperandrogenism, and metabolic dysfunction. Myo-inositol, a promising therapeutic alternative, may improve glucose and lipid metabolism through the 5′-adenosine monophosphate-activated protein kinase (AMPK)–glucose transporter type 4 (GLUT4) pathway. This study aimed to investigate the molecular and metabolic effects of Myo-inositol in a letrozole-induced rat model of PCOS.</p> Methods and results <p>We divided rats into six groups: controls, PCOS, and different doses of Myo-inositol- or metformin-treated groups. We examined the rat blood glucose, insulin, lipid profiles, and hormone levels alongside ovarian histology and AMPK/GLUT4 expression via polymerase chain reaction and western blotting assays. Myo-inositol treatment demonstrated dose-dependent improvements in glucose homeostasis, lipid profiles, and GLUT4 expression, with high-dose treatment reducing glucose by 0.85-fold and improving lipid metabolism compared to metformin treatment. Ovarian histology revealed partial restoration of follicular development, and AMPK activation supported enhanced glucose uptake.</p> Conclusions <p>Myo-inositol effectively alleviated insulin resistance and metabolic dysfunction, offering a promising alternative to conventional PCOS treatments.</p>

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Exploring the role of Myo-inositol in alleviating insulin resistance in polycystic ovary syndrome through the AMPK/GLUT4 pathway

  • 期刊论文

  • 发表日期：

    2025年5月13日

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  • Guihong Song,
  • Nannan Liu,
  • Jiajin He,
  • Saisai Tang,
  • Yiping Yu,
  • Lihua Song

摘要

Background

Polycystic ovary syndrome (PCOS) is a multifactorial disorder associated with insulin resistance, hyperandrogenism, and metabolic dysfunction. Myo-inositol, a promising therapeutic alternative, may improve glucose and lipid metabolism through the 5′-adenosine monophosphate-activated protein kinase (AMPK)–glucose transporter type 4 (GLUT4) pathway. This study aimed to investigate the molecular and metabolic effects of Myo-inositol in a letrozole-induced rat model of PCOS.

Methods and results

We divided rats into six groups: controls, PCOS, and different doses of Myo-inositol- or metformin-treated groups. We examined the rat blood glucose, insulin, lipid profiles, and hormone levels alongside ovarian histology and AMPK/GLUT4 expression via polymerase chain reaction and western blotting assays. Myo-inositol treatment demonstrated dose-dependent improvements in glucose homeostasis, lipid profiles, and GLUT4 expression, with high-dose treatment reducing glucose by 0.85-fold and improving lipid metabolism compared to metformin treatment. Ovarian histology revealed partial restoration of follicular development, and AMPK activation supported enhanced glucose uptake.

Conclusions

Myo-inositol effectively alleviated insulin resistance and metabolic dysfunction, offering a promising alternative to conventional PCOS treatments.