Pathogenesis of obstetric and perinatal complications in metabolic syndrome

Aim. To describe a pathogenetic rationale for obstetric and perinatal complications associated with metabolic syndrome. Materials and Methods. This is a descriptive review based on original research and review articles on obstetric and perinatal complications in the context of metabolic syndrome, published between 2016 and 2025 and indexed in PubMed, ScienceDirect, and eLibrary databases. The following research methods were employed: internet-based analysis, content analysis, historical method, and descriptive-analytical approach. Results . Obesity and metabolic syndrome have a negative impact on maternal and fetal outcomes. Adipose tissue functions as an active endocrine organ that regulates vascular, metabolic, and inflammatory processes across multiple organ systems, thereby affecting obstetric and perinatal outcomes. Conclusion. The obesity epidemic has drawn attention to adipose tissue as a critical regulator of systemic nutrient and energy homeostasis. In metabolic syndrome, adipose tissue must adapt to excessive lipid load through a variety of strategies, including increasing adipocyte size and number, altering immune cell composition, and reshaping lipid metabolism. Failure to adequately adapt to increased nutritional load results in adipose tissue dysfunction which triggers a cascade of lipotoxic effects on other organs, leading to insulin resistance, diabetes mellitus, and related metabolic complications. Adipose tissue dysfunction is significantly accelerated by the additional metabolic load imposed by pregnancy