High glycemic diet-induced mitochondrial dysfunction and female fertility: emerging molecular links between nutrition and reproductive health
- International Journal of Molecular Biology: Open Access
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Dr Palak Sangal
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Abstract
Female fertility is highly dependent on optimal mitochondrial function, as mitochondria regulate ATP generation, calcium homeostasis, redox signaling, and apoptosis in oocytes (female egg cells).1,2 Emerging evidence suggests that chronic consumption of high glycemic index (HGI) diets contributes to insulin resistance, oxidative stress, and mitochondrial dysfunction, ultimately impairing reproductive outcomes.3,4 Elevated postprandial glucose and hyperinsulinemia increase reactive oxygen species (ROS) production, disrupt mitochondrial membrane potential, damage mitochondrial DNA (mtDNA), and impair oocyte maturation.4,5 These metabolic disturbances are strongly associated with reproductive disorders such as polycystic ovary syndrome (PCOS), anovulation, poor embryo quality, and infertility.1,6 Furthermore, mitochondrial dysfunction activates apoptotic pathways in granulosa cells and compromises follicular development.5 Recent clinical and experimental studies indicate that low glycemic dietary interventions may improve insulin sensitivity, androgen profiles, and reproductive outcomes in women with metabolic infertility.6,7 This review summarizes current evidence linking high glycemic diets to mitochondrial dysfunction and female infertility and highlights potential nutritional strategies targeting mitochondrial health to improve reproductive outcomes.
Keywords
mitochondrial, infertility, stress


