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. Author manuscript; available in PMC: 2012 Nov 1.
Published in final edited form as: Gastroenterology. 2011 Sep 12;141(5):1572–1585. doi: 10.1053/j.gastro.2011.09.002

Figure 2.

Figure 2

Mechanisms of alcoholic fatty liver. (1) Alcohol consumption can directly (via acetaldehyde) or indirectly (via regulation of multiple factors) up-regulate the expression of SREBP-1c and down-regulate the expression of PPAR-α, leading to the induction of fatty acid synthesis and inhibition of fatty liver β-oxidation, which results in the development of alcoholic fatty liver. Alcohol exposure also inhibits AMPK and subsequently increases ACC activity but decreases carnitine palmitoyltransferase 1 (CPT-1) activity, leading to an increase in fatty acid synthesis and a decrease in fatty acid β-oxidation. (2) Alcohol consumption can also modify many factors, including HIF-1, C3, C1qa, PKC[H9255], and iNOS, that subsequently contribute to the development of fatty liver. The mechanisms underlying the effects of these factors remain unclear.