ROLE OF APOE GENE POLYMORPHISM IN THE DEVELOPMENT OF METABOLIC SYNDROME DURING MENOPAUSE

Abstract

Menopause represents a critical biological transition accompanied by profound endocrine restructuring and progressive metabolic vulnerability. Although estrogen deprivation is a fundamental trigger of metabolic disturbances, interindividual variability in cardiometabolic outcomes suggests a decisive role of inherited molecular determinants. Among genetic factors, the apolipoprotein E (APOE) gene occupies a central position due to its regulatory influence on lipid transport, remnant clearance, inflammatory modulation, and metabolic homeostasis.

This paper explores the mechanistic contribution of APOE polymorphic variants (ε2, ε3, ε4) to the development of metabolic syndrome in menopausal women. Special emphasis is placed on genotype-specific lipid handling, insulin signaling interference, adipose tissue remodeling, mitochondrial efficiency, and gene–environment interaction. The menopausal decline in estrogen is analyzed as a biological amplifier of genetically predetermined metabolic risk.

Understanding APOE-dependent metabolic heterogeneity may provide a foundation for precision-based preventive and therapeutic strategies in menopausal medicine.