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Fig. 6 | Lipids in Health and Disease

Fig. 6

From: Ethanol-mediated upregulation of APOA1 gene expression in HepG2 cells is independent of de novo lipid biosynthesis

Fig. 6

Major metabolic pathways of ethanol in humans. (Adapted from [23, 36, 38]). Orally ingested alcohol (EtOH) is rapidly oxidized in the liver to acetaldehyde, primarily by alcohol dehydrogenase(s), and secondarily by the microsomal ethanol oxidizing system (MEOS, including cytochrome P450 CYP2E1) or by peroxisomal catalase. Acetaldehyde is further rapidly oxidized to acetate, which is either converted directly to acetyl-CoA in the liver, or released to plasma, from where it is ultimately metabolized primarily to CO2 in peripheral tissues. Most ethanolic carbon is ultimately released as CO2. A small fraction of ethanolic carbon in acetyl-CoA is converted to free fatty acids (FFA) or cholesterol (cholest) via de novo lipid synthesis. A small fraction of ingested ethanol may be non-oxidatively metabolized to fatty acid ethyl ester (FAAE) or phosphatidyl ethanol (PTE). Acetyl-CoA synthetase 2 (ACSS2) also transfers acetate to chromosomal histones [39]. Octagons around EtOH and FFA/cholest denote that inhibitor studies indicate that these are not candidates for primary signaling molecules for ApoA1 upregulation

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