Study of Epicardial Fat Lipid in Coronary Heart Disease on the Regulation Mechanism of Metabolism

Abstract

Objective: Coronary heart disease (CHD), emerging as a common chronic disease, is threatening the lives of middle-aged and older people in China, with a gradual increase in morbidity and mortality. However, the metabolic mechanism of CHD remains unclear, necessitating a comprehensive elucidation. Therefore, this study aimed to examine the underlying regulatory mechanism of epicardial lipid metabolism in CHD. Methods: This study collected epicardial adipose tissue samples (n = 40), including 20 patients with CHD and 20 non-CHD. 3T3L1 was induced to differentiate into mature adipocytes in vitro and subsequently treated with different concentrations of oxidized low-density lipoprotein (ox-LDL), glucose, and lipopolysaccharide (LPS). The contents of glycerol and triglyceride were determined using corresponding kits. Moreover, the concentrations of cyclic adenosine monophosphate (cAMP) and protein kinase A (PKA) were assessed utilizing ELISA. Furthermore, western blotting analysis and qRT-PCR were employed to determine protein and mRNA expression levels. Additionally, immunofluorescence analysis was utilized to assess the expression of lipid droplet coating protein perilipin A. The morphology and count of lipid droplets were observed using a confocal microscope. Results: Compared to the non-CHD group, the level of triglyceride and perilipin A increased significantly, while the content of glycerol, PKA, cAMP, adipose triglyceride lipase (ATGL), and hormone-sensitive lipase (HSL) decreased in the CHD group. Furthermore, high ox-LDL and glucose significantly decreased small lipid droplets, glycerol, ATGL, and HSL while substantially increasing large lipid droplets, triglyceride, cAMP, PKA, and perilipin A in 3T3L1 cells. Additionally, high LPS concentration significantly increased small lipid droplets, glycerol, cAMP, PKA, ATGL, and HSL, and decreased large lipid droplets, triglyceride, and perilipin A. Conclusions: In summary, high ox-LDL and glucose levels regulate the lipolysis of 3T3L1 adipocytes by regulating the cAMP-PKA and perilipin A-ATGL-HSL pathways. However, high LPS can promote the hydrolysis of 3T3L1 adipocytes.