Abstract
Backgroundː Numerous in vivo human cohort studies have suggested that the apolipoprotein B100/apolipoprotein AI (ApoB100/ApoAI) ratio might be a risk factor in coronary heart disease. The aim of this study was to measure ApoB100/ApoAI ratio changes in cell secretions by incubating HepG2 cells with various amounts of glucose in vitro. Methods ː HepG2 cells were cultured in low-, normal- or high-glucose Dulbecco's Modified Eagle Medium (DMEM) (1, 4.5 and 10g/L, respectively). Levels of ApoAI and ApoB100 were measured with commercial sandwich enzyme-linked immunosorbent assay kits (cat#: H0123 and H0124) from ShangHai MEIXUAN Biological Science and Technology Ltd (Shanghai, China). Experiments were repeated six times for each assay. Resultsː The results showed that ApoB100/ApoAI ratio have positive correlations with the glucose concentration increase. Conclusionsː A higher concentration of glucose induced an undesirable ApoB100/ApoAI ratio change, which suggests a new regulatory pathway in lipoprotein catabolism and provides a cell model for further mechanism study. This finding may lead to novel therapeutic ways for diagnosis and treatment for coronary artery disease.
Highlights
Atherosclerotic coronary artery occlusion is the most frequent cause of coronary heart disease (CHD); numerous epidemiologic studies and randomized clinical trials have established that lipoprotein metabolism is a major contributor to CHD.[1]
In order to prove those in vivo human cohort findings that ApoB100/Apolipoprotein AI (ApoAI) ratio is a CHD risk factor and understand the molecular mechanism of how ApoB100/ApoAI ratios are modulated in atherosclerosis, an in vitro cell assay model was built in the current study
Glucose modulates secretion of ApoB100 and ApoAI in HepG2 cells To explore the impacts of glucose on ApoB100 and ApoAI secretion over different concentrations, HepG2 cells were exposed to low (1 g/L), medium (4.5 g/L) and high (10 g/L) concentrations of glucose
Summary
Atherosclerotic coronary artery occlusion is the most frequent cause of coronary heart disease (CHD); numerous epidemiologic studies and randomized clinical trials have established that lipoprotein metabolism is a major contributor to CHD.[1] Conventionally, it was thought that increases in plasma low-density lipoprotein cholesterol (LDL-C) and decreases in high-density lipoprotein cholesterol (HDL-C) were the major factors causing CHD.[2] numerous in vivo human cohort studies have suggested that another factor in CHD risk might be the apolipoprotein B100/ apolipoprotein AI (ApoB100/ApoAI) ratio.[3,4,5,6,7]. Numerous in vivo human cohort studies have suggested that the apolipoprotein B100/apolipoprotein AI (ApoB100/ApoAI) ratio might be a risk factor in coronary heart disease.
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