Beer Is Less Harmful for the Liver than Plain Ethanol
Beer Is Less Harmful for the Liver than Plain Ethanol
Aims Mechanisms involved in the less damaging effects of beer in comparison to hard spirits have not yet been fully understood. The aim of the study was to determine if the effect of beer intake on the liver differs from that of plain ethanol and if so to determine mechanisms involved.
Methods Male C57BL/6J mice received either ethanol, beer (ethanol content: 6 g/kg body weight) or iso-caloric maltodextrin solution. Markers of steatosis, lipogenesis, activation of the toll-like receptor-4 signaling cascade and lipid export in liver and tight junction proteins in duodenum were measured 6 and 12 h after acute ethanol or beer intake.
Results Alcohol ingestion resulted in a significant increase of hepatic triglyceride accumulation 6 and 12 h after ingestion, respectively, being markedly lower in mice fed beer. Expression of sterol regulatory element-binding protein-1c mRNA was significantly lower 12 h after alcohol or beer exposure, while fatty acid synthase mRNA expression was induced in livers of ethanol-fed mice and to a lesser extent in mice fed beer 6 h after acute alcohol ingestion. Protein levels of tight junction proteins in the small intestine were similar between groups while expression of myeloid differentiation primary response gene 88 in livers was significantly induced in ethanol- but not in beer-fed mice. Concentrations of 4-hydroxynonenal protein adducts and inducible nitric oxide synthase protein were also only induced in livers of mice fed ethanol. Protein levels of apolipoprotein B were induced in livers of beer-fed mice only.
Conclusion Our data suggest that beer is less harmful on the development of acute alcohol-induced liver damage than plain ethanol in male mice.
Chronic alcohol abuse is still one of the leading causes of liver associated diseases but also mortality worldwide (Rehm et al., 2013). However, results of epidemiological studies also suggest that the impact of alcoholic beverages on the liver might differ. Indeed, results of epidemiological studies suggest that chronic consumption of hard spirits might be more harmful to the liver than that of fermented alcoholic beverages (Kerr et al., 2000; Ponicki and Gruenewald, 2006). In line with these findings, beer constituents like xanthohumol but also iso-acids have been shown to at least in part attenuate hepatic inflammation and fibrosis (Stevens and Page, 2004; Dorn et al., 2010). Furthermore, studies using alcohol-free beer also found beneficial effects on markers associated with liver health (i.e. markers of lipid peroxidation) (Martinez Alvarez et al., 2009). In a recent study of our own group we found that in female mice, shown to be more susceptible to alcohol-induced liver damage, the damaging effects of beer on the liver were less pronounced when compared to equal doses of plain ethanol (Kanuri et al., 2014); however, molecular mechanisms underlying this less damaging effect of beer on the liver but also eventual gender-specific differences have not been clarified yet.
To study molecular mechanisms of early stages of alcohol-induced liver damage, animal-based models have been found to be useful tools, as they resemble many alterations found in humans with alcoholic liver disease (for overview see Bergheim et al., 2011). As rodent models of acute alcohol ingestion and chronic intake have been shown before (Enomoto et al., 2000; Bergheim et al., 2006) to share similar mechanisms, mouse models of acute alcohol consumption are useful tools to mimic the very early alterations associated with high alcohol intake (i.e. like the activation of nuclear factor kappa B (NFκB) and formation of reactive oxygen species (ROS) as well as an increased translocation of bacterial endotoxin from the gut).
Starting from this background the aim of the present study was to determine if beer possesses a less harmful effect on livers of male mice in a mouse binge-drinking model, and if so, to further unravel molecular mechanisms involved.
Abstract and Introduction
Abstract
Aims Mechanisms involved in the less damaging effects of beer in comparison to hard spirits have not yet been fully understood. The aim of the study was to determine if the effect of beer intake on the liver differs from that of plain ethanol and if so to determine mechanisms involved.
Methods Male C57BL/6J mice received either ethanol, beer (ethanol content: 6 g/kg body weight) or iso-caloric maltodextrin solution. Markers of steatosis, lipogenesis, activation of the toll-like receptor-4 signaling cascade and lipid export in liver and tight junction proteins in duodenum were measured 6 and 12 h after acute ethanol or beer intake.
Results Alcohol ingestion resulted in a significant increase of hepatic triglyceride accumulation 6 and 12 h after ingestion, respectively, being markedly lower in mice fed beer. Expression of sterol regulatory element-binding protein-1c mRNA was significantly lower 12 h after alcohol or beer exposure, while fatty acid synthase mRNA expression was induced in livers of ethanol-fed mice and to a lesser extent in mice fed beer 6 h after acute alcohol ingestion. Protein levels of tight junction proteins in the small intestine were similar between groups while expression of myeloid differentiation primary response gene 88 in livers was significantly induced in ethanol- but not in beer-fed mice. Concentrations of 4-hydroxynonenal protein adducts and inducible nitric oxide synthase protein were also only induced in livers of mice fed ethanol. Protein levels of apolipoprotein B were induced in livers of beer-fed mice only.
Conclusion Our data suggest that beer is less harmful on the development of acute alcohol-induced liver damage than plain ethanol in male mice.
Introduction
Chronic alcohol abuse is still one of the leading causes of liver associated diseases but also mortality worldwide (Rehm et al., 2013). However, results of epidemiological studies also suggest that the impact of alcoholic beverages on the liver might differ. Indeed, results of epidemiological studies suggest that chronic consumption of hard spirits might be more harmful to the liver than that of fermented alcoholic beverages (Kerr et al., 2000; Ponicki and Gruenewald, 2006). In line with these findings, beer constituents like xanthohumol but also iso-acids have been shown to at least in part attenuate hepatic inflammation and fibrosis (Stevens and Page, 2004; Dorn et al., 2010). Furthermore, studies using alcohol-free beer also found beneficial effects on markers associated with liver health (i.e. markers of lipid peroxidation) (Martinez Alvarez et al., 2009). In a recent study of our own group we found that in female mice, shown to be more susceptible to alcohol-induced liver damage, the damaging effects of beer on the liver were less pronounced when compared to equal doses of plain ethanol (Kanuri et al., 2014); however, molecular mechanisms underlying this less damaging effect of beer on the liver but also eventual gender-specific differences have not been clarified yet.
To study molecular mechanisms of early stages of alcohol-induced liver damage, animal-based models have been found to be useful tools, as they resemble many alterations found in humans with alcoholic liver disease (for overview see Bergheim et al., 2011). As rodent models of acute alcohol ingestion and chronic intake have been shown before (Enomoto et al., 2000; Bergheim et al., 2006) to share similar mechanisms, mouse models of acute alcohol consumption are useful tools to mimic the very early alterations associated with high alcohol intake (i.e. like the activation of nuclear factor kappa B (NFκB) and formation of reactive oxygen species (ROS) as well as an increased translocation of bacterial endotoxin from the gut).
Starting from this background the aim of the present study was to determine if beer possesses a less harmful effect on livers of male mice in a mouse binge-drinking model, and if so, to further unravel molecular mechanisms involved.
