Abstract
The present study tested the hypothesis that Korean red ginseng (KRG) provides a protective effect against alcoholic fatty liver. Male Sprague-Dawley rats were divided into four groups and fed a modified Lieber-DeCarli diet containing 5% (w/v) alcohol or an isocaloric amount of dextrin-maltose for the controls for 6 weeks: normal control (CON), alcohol control (ET), and ET treated with 125 or 250 mg/kg body weight/day of KRG (RGL or RGH, respectively). Compared with the CON group, the ET group exhibited a significant increase in triglycerides, total cholesterol and the presence of lipid droplets in the liver, and a decrease in fat mass, which were all attenuated by KRG supplementation in adose-dependent manner. The mitigation was accompanied by AMP-activated protein kinase (AMPK) signaling pathways in the liver and adipose tissue. In addition, suppression in the alcohol-induced changes of adipose adipokine mRNA expression was also observed in KRG supplementation group. These findings suggest that KRG may have the potential to ameliorate alcoholic fatty liver by suppressing inappropriate lysis of adipose tissue and preventing unnecessary de novo lipogenesis in the liver, which are mediated by AMPK signaling pathways. A mechanism for an interplay between the two organs is still needed to be examined with further assays.
Highlights
Alcoholic liver disease remains one of the most common etiologies of liver disease and has become a major cause of morbidity and mortality worldwide [1]
Considering that adipose tissue plays an important role as a major metabolic buffering system for lipid metabolic homeostasis [9,10], modification of alcohol-induced dysfunction in adipose tissue might be an important target for development of functional foods to prevent alcoholic fatty liver [9,11]
Alcohol was provided at 5% of the Lieber-DeCarli liquid diet, and Korean red ginseng (KRG) was administered daily by gavage for the same time period
Summary
Alcoholic liver disease remains one of the most common etiologies of liver disease and has become a major cause of morbidity and mortality worldwide [1]. Considering that adipose tissue plays an important role as a major metabolic buffering system for lipid metabolic homeostasis [9,10], modification of alcohol-induced dysfunction in adipose tissue might be an important target for development of functional foods to prevent alcoholic fatty liver [9,11]. The effects of KRG on alcohol-induced dysregulation of lipid homeostasis and the underlying mechanism(s) responsible for it remain un addressed. We tested a hypothesis that KRG may have the potential to protect against alcoholic fatty liver To test this hypothesis, we determined lipid profiles in plasma and the liver and made a histological observation in the liver of rats fed Lieber-DeCarli Diets containing 5% (w/v) alcohol. To explore the underlying mechanism, we compared the changes in AMPK signaling pathways in the liver and adipose tissue
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