Abstract:

Metabolic syndrome has become a defining global health burden of the 21st century, arising from the increasing prevalence of obesity, sedentary behavior, and poor dietary patterns. Contemporary evidence demonstrates that obesity initiates a cascade of metabolic and molecular disturbances involving hormonal dysregulation, inflammatory signaling, and altered energy metabolism that culminate in cardiovascular disease. Despite extensive studies, the mechanistic transition linking excess adiposity to molecular dysfunction and cardiovascular pathology remains incompletely understood, with limited integration of genetic, microbial, and biochemical perspectives. This study examines how body recomposition and metabolic regulation interact to transform excess body weight into systemic molecular disruptions, emphasizing the roles of adipokines, gut microbiota, and mitochondrial homeostasis in cardiovascular deterioration. The synthesis of recent findings indicates that imbalances in leptin, ghrelin, and cortisol; genetic variations in PPAR-γ and FTO; and gut microbiome dysbiosis collectively drive chronic inflammation, oxidative stress, and endothelial injury, forming the core mechanism of cardiometabolic decline. By integrating hormonal, genetic, and microbial dimensions, the study reframes metabolic syndrome as a continuum of molecular maladaptations rather than an isolated metabolic disorder. These insights highlight the need for precision-based, integrative strategies focusing on restoring metabolic homeostasis rather than solely reducing body weight, thereby redefining prevention and management of cardiometabolic diseases in the modern era.