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Chronic ethanol-induced downregulation of peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1 α ) and upregulation of peroxisome proliferator-activated receptor gamma coactivator 1-beta (PGC1 β ) affect hepatic lipid oxidation and lipogenesis, respectively, leading to fatty liver injury. Low- ω 3 fatty acid (Low- ω 3FA) that primarily regulates PGC1 α  and soy protein (SP) that seems to have its major regulatory effect on PGC1 β  were evaluated for their protective effects against ethanol-induced hepatosteatosis in rats fed with Lieber-deCarli control or ethanol liquid diets with high or low  ω 3FA fish oil and soy protein. Low- ω 3FA and SP opposed the actions of chronic ethanol by reducing serum and liver lipids with concomitant decreased fatty liver. They also prevented the downregulation of hepatic Sirtuin 1 (SIRT1) and PGC1 α  and their target fatty acid oxidation pathway genes and attenuated the upregulation of hepatic PGC1 β  and sterol regulatory element-binding protein 1c (SREBP1c) and their target lipogenic pathway genes  via  the phosphorylation of 5′ adenosine monophosphate-activated protein kinase (AMPK). Thus, these two novel modulators attenuate ethanol-induced hepatosteatosis and consequent liver injury potentially by regulating the two opposing lipid oxidation and lipogenic pathways.

oxidative medicine and cellular longevity

Low-<i>ω</i>3 Fatty Acid and Soy Protein Attenuate Alcohol-Induced Fatty Liver and Injury by Regulating the Opposing Lipid Oxidation and Lipogenic Signaling Pathways

Low-ω3 Fatty Acid and Soy Protein Attenuate Alcohol-Induced Fatty Liver and Injury by Regulating the Opposing Lipid Oxidation and Lipogenic Signaling Pathways