Polycystic ovary syndrome (PCOS) is a prevalent and complex endocrine disorder affecting 4–20% of women of reproductive age worldwide. It is characterized by dyslipidemia, insulin resistance, weight gain, and increased risk of cardiovascular disease. An imbalance in the hypothalamic-pituitary-ovarian axis is an important pathophysiological basis of PCOS. Lactate, a glycolytic product and an important energy source, also regulates gene transcription through histone lactylation, a novel post-translational modification. Emerging evidence highlights the crucial role of lactate and lactylation in cancer, inflammation, and metabolic reprogramming, although the exact mechanisms remain unclear. Based on the manifestations of PCOS, we hypothesized a potential link between lactate levels, lactylation, and PCOS. This review explores the role of lactate in PCOS pathophysiology, examines the regulatory effect of metabolic reprogramming on various pathophysiological scenarios, and discusses the therapeutic potential of targeting lactate metabolism in PCOS management.
Keywords: Inflammation; Insulin resistance; Lactate metabolism; Metabolic reprogramming; PCOS.