earticle

영어

Macrophages foam cell formation is characterized by lipid accumulation and plays a key role in early atherogenesis. In this study, we showed that glucosamine dose dependently stimulated lipid accumulation in RAW 264.7 cells. In addition, glucosamine synergistically promoted oleic acid-induced lipid accumulation. Sterol regulatory element-binding proteins (SREBPs) have been described as key transcription factors for lipogenic gene induction. Glucosamine enhanced DNA binding activity on SRE/E-box of SREBP-1 and mRNA expression of this target genes Acetyl-CoA carboxylase (ACC) and Fatty acid synthas (FAS). Since SREBP transcription activity is regulated by mammalian target of rapamycin (mTOR), we examined the effect of mTORC1-specific inhibitor, rapamycin on glucosamine-induced lipid accumulation; Glucosamine-induced lipid accumulation was suppressed by rapamycin. Although glucosamine promoted the endoplasmic reticulum stress marker, glucose-regulated protein-78 (GRP78) protein and mRNA level, glucosamine-induced lipid accumulation dose not suppressed by ER stress inhibitor 4-phenylbutyric acid (PBA). This suggest that glucosamine-induced lipid accumulation were not likely mediated with ER stress.