Mediators of steatosis in HepG2 cells

Hepatic lipid accumulation or steatosis has become nowadays a major public health problem. The disease can progress into serious liver damage that can lead eventually to hepatic failure and cancer. Fatty liver may result from an increase in lipid acquisition or a decrease in lipid disposal, or both. Although lipid metabolism is known to be under the control of multiple enzymes and signaling molecules, the ones dysregulated in steatosis are still ill defined. The aim of this study was to identify the key molecules altered during hepatic lipid accumulation. Steatosis was induced by incubating HepG2 cells for 24 hrs with 1 mM Oleic and Palmitic acid. Cellular lipid content was quantified using a lipid extraction kit in which lipids were stained with Oil red O, then extracted and quantified colorimetrically. The fatty acids, which are known to activate Gq-linked fatty acid receptors, increased significantly lipid accumulation. This increase was not maintained in presence of specific inhibitors of Gq, PI3K, mTOR, SREBP, and PPARϒ. Gq was found to be upstream of all the other intermediates. It was concluded that saturated fatty acids activate a Gq signaling pathway involving kinases and transcription factors implicated in lipogenesis. The location of the different intermediates with respect to each other needs still to be determined. University Research Board- American University of Beirut This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.