PMID: 22347525Feb 22, 2012Paper

Pharmacological ER stress promotes hepatic lipogenesis and lipid droplet formation.

American Journal of Translational Research
Jin-Sook LeeKezhong Zhang

Abstract

Endoplasmic Reticulum (ER) stress refers to a condition of accumulation of unfolded or misfolded proteins in the ER lumen. A variety of biochemical stimuli or pathophysiologic conditions can directly or indirectly induce ER stress, leading to activation of an ER-originated adaptive signaling response called Unfolded Protein Response (UPR). Recent studies demonstrated that ER stress and UPR signaling are critically involved in the initiation and progression of many diseases, such as metabolic disease, cardiovascular disease, neurodegenerative disease, and cancer. In this study, we show that ER stress induced by pharmacologic reagents, including tunicamycin (TM) and thapsigargin (Tg), promotes hepatic lipogenesis and lipid droplet formation. Using quantitative gene expression analysis, we identified 3 groups of key lipogenic regulators or enzymes that are inducible by pharmacological ER stress in a human hepatoma cell line Huh-7. These ER stress-inducible lipogenic factors include: 1) lipogenic trans-activators including CCAAT/ enhancer binding protein alpha (C/EBPα), peroxisome proliferator-activated receptor gamma (PPARγ), PPARγ coacti-vator 1-alpha (PGC1α), and Liver X receptor alpha (LXRα); 2) components of lipid droplets inc...Continue Reading

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