Maternal Metabolic Dysfunction and Uteroplacental Adaptation in Polyendocrine Metabolic Ovarian Syndrome Pregnancy
Abstract
Polyendocrine metabolic ovarian syndrome (PMOS), formerly known as polycystic ovary syndrome (PCOS), is a multisystem endocrine-metabolic disorder that significantly increases the risk of adverse pregnancy outcomes, partly independently of obesity. PMOS patients frequently exhibit a characteristic metabolic-endocrine milieu of insulin resistance, hyperandrogenemia, dyslipidemia, and chronic low-grade inflammation. The physiological insulin resistance of pregnancy, driven by placental hormones, exacerbates these pre-existing disturbances and disrupts endometrial receptivity and placental function. These insults converge on conserved signaling pathways, phosphoinositide 3-kinase (PI3K)/ protein kinase B (AKT)/ mechanistic target of rapamycin (mTOR), nuclear factor kappa B (NF-κB)/ c-Jun N-terminal kinase (JNK), androgen receptor-mediated mitochondrial dysfunction and ferroptosis, and peroxisome proliferator-activated receptor (PPAR)-regulated lipid dysregulation, and impair trophoblast invasion, spiral artery remodeling, angiogenic balance, and nutrient transport. The resulting mitochondrial oxidative stress and lipotoxic injury contribute to early pregnancy loss, gestational diabetes, hypertensive disorders, preterm birth, and aberrant fetal growth. Concurrently, the dysmetabolic intrauterine environment programs offspring metabolic and reproductive dysfunction through epigenetic and developmental mechanisms. This review synthesizes current evidence linking the maternal…
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