Fig. 1.

Interactions between ethanol, transcriptional controls of lipid metabolism, and endoplasmic reticulum (ER) stress in the liver. PPARα, peroxisome proliferator-activated receptor-α; MTP, microsomal triglyceride transfer protein; AMPK, AMP-activated protein kinase; SREBP-1, sterol response element-binding protein-1; ACC, acetyl-CoA carboxylase. Consumption of ethanol inhibits regulatory systems that are needed to promote the oxidation of fatty acids (PPARα and AMPK) and activates the systems that stimulate fatty acid synthesis (SREBP-1, in part via activation of the ER stress response). The ER stress response also increases the likelihood that hepatocytes will undergo apoptosis.