BIOCHEMICAL FOUNDATIONS OF THE DEVELOPMENT OF METABOLIC SYNDROME AND ITS COMPLICATIONS

Metabolic syndrome (MetS) is a complex metabolic disorder characterized by a cluster of interconnected conditions, including insulin resistance, central obesity, dyslipidemia, hypertension, and impaired glucose metabolism. The biochemical foundations of MetS involve disturbances in carbohydrate and lipid metabolism, chronic low-grade inflammation, oxidative stress, and hormonal imbalance. Insulin resistance plays a central role in the pathogenesis of the syndrome, leading to altered glucose uptake, increased free fatty acid levels, and endothelial dysfunction. These biochemical alterations contribute to the development of severe complications such as type 2 diabetes mellitus, cardiovascular diseases, non-alcoholic fatty liver disease, and chronic kidney disease [1,2]. Recent research highlights the importance of adipokines, inflammatory cytokines, mitochondrial dysfunction, and oxidative damage in the progression of metabolic syndrome and its systemic consequences [3,4]. Understanding the molecular and biochemical mechanisms underlying MetS is crucial for early diagnosis, prevention, and the development of targeted therapeutic strategies aimed at reducing morbidity and mortality associated with this condition.代谢综合征（Metabolic syndrome, MetS）是一类复杂的代谢紊乱性疾病，以一组相互关联的病症集群为特征，涵盖胰岛素抵抗（insulin resistance）、中心性肥胖（central obesity）、血脂异常（dyslipidemia）、高血压（hypertension）及糖代谢受损（impaired glucose metabolism）。其生化基础涉及糖脂代谢紊乱、慢性低度炎症、氧化应激及激素失衡。其中，胰岛素抵抗在该综合征的发病机制中居于核心地位，可导致葡萄糖摄取异常、游离脂肪酸水平升高及内皮功能障碍。上述生化改变会推动严重并发症的发生发展，例如2型糖尿病（type 2 diabetes mellitus）、心血管疾病（cardiovascular diseases）、非酒精性脂肪肝病（non-alcoholic fatty liver disease）及慢性肾脏病（chronic kidney disease）[1,2]。 近期研究凸显了脂肪因子（adipokines）、炎症细胞因子（inflammatory cytokines）、线粒体功能障碍（mitochondrial dysfunction）及氧化损伤（oxidative damage）在代谢综合征进展及其全身并发症中的关键作用[3,4]。阐明代谢综合征背后的分子与生化机制，对于该疾病的早期诊断、预防，以及研发旨在降低其相关发病率与死亡率的靶向治疗策略，均具有至关重要的意义。