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. 2017 Sep 25;9(10):130. doi: 10.3390/cancers9100130

Figure 2.

Figure 2

Metabolic effects of alcohol exposure on hepatocytes. Ethanol consumption directly and indirectly enhances lipid accumulation in hepatocytes via promoting the transcriptional activity of SREBP-1 and PPAR-γ. Acetaldehyde and ER stress also contribute to steatosis by inducing SREBP-1 activity and inhibiting PPAR-α expression. Moreover, alcohol metabolism increases ROS production via induction of CYP2E1 and impairment of mitochondrial functionality. Acetaldehyde and ROS exerts cyto-toxicity through generation of protein/DNA adducts and lipid peroxidation. ACC1: Acetyl-CoA-carboxylase-1; FASN: Fatty acid synthase; SCD1: Stearoyl-CoA desaturase-1; CPT1a: Carnitine Palmitoyltransferase 1a; CD36: Cluster of differentiation 36; MGAT1: Mannosyl(alpha-1,3)-glycoprotein beta-1,2-N-Acetylglucosaminyltransferase.