Abstract
Dexamethasone (DEX) is a synthetic glucocorticoid with anti-inflammatory properties. We evaluated a potentially protective dexamethasone influence on hepatocellular lipid metabolism and fatty acid (FA) transporters expression. The HepG2 cells were incubated with palmitic acid (PA) and/or dexamethasone in two different time expositions (16 h and 40 h). Intracellular and extracellular lipid and sphingolipid concentrations were estimated by the gas-liquid chromatography and high-performance liquid chromatography, respectively. The protein expression involved in FA uptake and lipid metabolism was determined by immunoblotting. The treatment of HepG2 with dexamethasone and palmitate enhanced lipid transport to the cell via increased especially FABPpm expression and resulted in the increased triacylglycerol (TAG), diacylglycerol (DAG) and ceramide deposition. Dexamethasone with palmitate treatment altered FA composition resulting in the elevated n-3 polyunsaturated fatty acid (PUFA) activity in DAG and TAG and the diminished n-6 PUFA activity in DAG after prolonged exposure. We may speculate that although protective lipid secretion into media and decrease in inflammatory FA precursors dexamethasone treatment exacerbated lipotoxicity in HepG2 cells.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callMore From: Biochemical and Biophysical Research Communications
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
