Transcriptomic analysis of nuclear receptor(LXR, FXR) modulation, mTOR inhibition, and nutrient stress on human HepG2 cells

Bile acids (BAs), via the nuclear receptor FXR, regulate a complex transcriptional program to maintain fat, glucose, and protein metabolism. The mTORC1 signalling pathway integrates diverse nutrient/hormonal signals into FXR-related metabolic outputs, raising the question whether these transcriptional and posttranslational cascades are intertwined to maintain cellular homeostasis. Human HepG2 cells were treated with LXR agonist (GW3965), FXR agonist (GW4064) alone or combined with mTORC1 inhibitor Torin 1 (TOI), or combined with glucose/glutamine starved media (GLUST).