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）是一类由多种相互关联的代谢异常病症组成的复杂代谢紊乱症候群，涵盖胰岛素抵抗、中心性肥胖、血脂异常、高血压及糖代谢受损等表现。其生化基础涉及糖脂代谢紊乱、慢性低度炎症、氧化应激与激素失衡。胰岛素抵抗在该综合征的发病机制中居于核心地位，可引发葡萄糖摄取异常、游离脂肪酸水平升高及内皮功能障碍。上述生化改变会促使严重并发症的发生，包括2型糖尿病、心血管疾病、非酒精性脂肪性肝病以及慢性肾脏病[1,2]。 近期研究凸显了脂肪因子、炎性细胞因子、线粒体功能障碍及氧化损伤在代谢综合征进展及其全身并发症中的关键作用[3,4]。阐明代谢综合征的分子与生化机制，对于该病症的早期诊断、预防，以及开发旨在降低其相关发病率与死亡率的靶向治疗策略具有重要意义。