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.
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Reyes‐Gordillo et al. (2016) studied this question.