Obesity, a chronic metabolic disease prevalent worldwide, is closely associated with complications such as type 2 diabetes, metabolism-related fatty liver disease, and cardiovascular disease. The phosphatidylinositol-3-hydroxykinase (PI3K)/protein kinase B (Akt) signaling pathway is a core hub for regulating cell growth, metabolism, and insulin signal transduction, and its dysfunction is a key molecular mechanism driving the occurrence and development of obesity and its complications. Traditional Chinese medicine (TCM), with its multi-component, multi-target, and holistic regulatory features, has demonstrated unique potential in the prevention and treatment of obesity. This review systematically explains the molecular composition of the PI3K/Akt signaling pathway and its core regulatory role in the energy metabolism of multiple tissues, including adipose, liver, muscle, cardiovascular, pancreatic, and brain. It also deeply analyzes the pathological connection between this pathway and chronic inflammation, lipid metabolism imbalance, and abnormal cell proliferation in obesity. It also focuses on summarizing the active ingredients of TCM, such as saponins, flavonoids, alkaloids, terpenes, phenolic acids, and polysaccharides, as well as the pharmacological mechanisms of classic compound prescriptions in improving obesity through precise regulation of the PI3K/Akt pathway. Existing evidence shows that TCM can effectively regulate glucose and lipid metabolism, alleviate insulin resistance, and inhibit inflammation and oxidative stress by activating or inhibiting PI3K/Akt signaling, thereby intervening in obesity and its complications through multiple pathways. This provides an important theoretical basis and research direction for explaining the modern scientific connotation of metabolic regulation in TCM and promoting the development of targeted treatment strategies.

PI3K/Akt signaling pathway  /  obesity  /  traditional Chinese medicine  /  traditional Chinese medicine compound  /  insulin resistance  /  glucose and lipid metabolism  /  oxidative stress