Adipocytes play a critical role in maintaining systemic homeostasis under fluctuating nutritional conditions, such as feeding, fasting, and even starvation. They store excess energy in the form of triglycerides when energy supply is abundant, and mobilize and release these reserves during periods of deficiency.
However, chronic excess caloric intake and physical inactivity impair the intrinsic physiological functions of adipocytes, leading to pathological changes and dysregulated adipocytokine secretion. As a consequence, surplus energy is ectopically deposited in non-adipose tissues such as the liver, heart, and skeletal muscle, ultimately contributing to the development of metabolic syndrome.
Furthermore, this pathological state serves as a fundamental basis for severe cardiovascular diseases, including myocardial infarction and cerebral infarction.
Our research aims to elucidate the molecular mechanisms underlying both the normal physiological functions of adipocytes and the pathogenesis of obesity resulting from their dysfunction. Through this work, we seek to contribute to the development of novel diagnostic and preventive strategies for cardiovascular diseases.