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<p>In recent years, the global prevalence of obesity has witnessed a sharp increase. Abnormal body mass index (BMI) exerts a profound influence on female fertility, particularly on oocyte quality. This review systematically summarizes the correlation between abnormal BMI and oocyte quality. It focuses on the mechanisms through which obesity impairs oocytes by disrupting lipid metabolism, energy supply, oxidative stress, DNA damage and repair, as well as epigenetic regulation. Obesity disrupts lipid homeostasis in follicular fluid, thereby inducing lipotoxicity. It damages mitochondria and the endoplasmic reticulum, resulting in insufficient energy production. It triggers excessive oxidative stress, which impairs mitochondrial DNA integrity and meiosis. It aggravates DNA damage while weakening the repair capacity, and disturbs DNA methylation and histone modifications, thus posing a threat to oocyte genomic stability and the developmental health of offspring. Although low BMI is also associated with poor oocyte quality, relevant studies are scarce, limiting the coverage of low BMI in this review. Clinically, abnormal BMI reduces the rates of implantation and live birth and increases the risk of miscarriage. Future research ought to focus on the mechanisms by which obesity and underweight affect oocyte quality, formulate targeted interventions like weight management and antioxidant therapy, and refine personalized assisted reproductive strategies to enhance the reproductive outcomes of women with abnormal BMI.</p>

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A review of the association between abnormal body mass index and oocyte quality

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年6月1日

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  • Dan Lin,
  • Yang-Zi-Yu Tao,
  • Xin-Xin Lin,
  • Er-Juan Lin,
  • Bing-Bing Pan,
  • Ming-Ting Jiang,
  • Zhi-Ren Liu

摘要

In recent years, the global prevalence of obesity has witnessed a sharp increase. Abnormal body mass index (BMI) exerts a profound influence on female fertility, particularly on oocyte quality. This review systematically summarizes the correlation between abnormal BMI and oocyte quality. It focuses on the mechanisms through which obesity impairs oocytes by disrupting lipid metabolism, energy supply, oxidative stress, DNA damage and repair, as well as epigenetic regulation. Obesity disrupts lipid homeostasis in follicular fluid, thereby inducing lipotoxicity. It damages mitochondria and the endoplasmic reticulum, resulting in insufficient energy production. It triggers excessive oxidative stress, which impairs mitochondrial DNA integrity and meiosis. It aggravates DNA damage while weakening the repair capacity, and disturbs DNA methylation and histone modifications, thus posing a threat to oocyte genomic stability and the developmental health of offspring. Although low BMI is also associated with poor oocyte quality, relevant studies are scarce, limiting the coverage of low BMI in this review. Clinically, abnormal BMI reduces the rates of implantation and live birth and increases the risk of miscarriage. Future research ought to focus on the mechanisms by which obesity and underweight affect oocyte quality, formulate targeted interventions like weight management and antioxidant therapy, and refine personalized assisted reproductive strategies to enhance the reproductive outcomes of women with abnormal BMI.