Beer Is Less Harmful for the Liver than Plain Ethanol: Studies in Male Mice Using a Binge-Drinking Model

Landmann, Marianne; Wagnerberger, Sabine; Kanuri, Giridhar; Ziegenhardt, Doreen; Bergheim, Ina

doi:10.1093/alcalc/agv048

Cited by 15 publications

(13 citation statements)

References 22 publications

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“…This diet allows for alcohol consumption of clinical relevance and offers flexibility to adjust to special experimental or physiologic needs by allowing for various substitutions required for a particular experimental design, including changes in lipids, carbohydrates or other dietary constituents [35]. In contrast, alcohol administration in water is associated with insufficient consumption and heavy weight loss [22,36]. In our current study, we have found that rats of HF-EFr group consumed 10.0 g ethanol/kg BW/day per rat.…”

Section: Discussionmentioning

confidence: 99%

“…Beneficial effects of alcohol drinking [55] including enhancing insulin sensitivity and adiponectin levels in postmenopausal women [56], and preventing the onset of NAFLD in ob / ob mice have been reported [22,57]. Consumption of HFD decreased adiponectin expression in rodents [58].…”

Section: Discussionmentioning

confidence: 99%

“…This has been verified in human individuals subjected to a high-fructose diet for 7 days led to an increased lipid deposition in liver and muscle, and reduced hepatic insulin sensitivity [20,21]. Similarly, acute alcohol ingestion promotes the hepatic expression of lipogenic and pro-inflammatory genes and lipid peroxidation [22]. However, it is unclear whether hepatic steatosis directly causes T2DM, or metabolic dysfunction is responsible for steatosis, or an interaction of both is regulated to produce T2DM.…”

Section: Introductionmentioning

confidence: 94%

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Insulin Production and Resistance in Different Models of Diet-Induced Obesity and Metabolic Syndrome

Alwahsh

Dwyer

Forbes

et al. 2017

IJMS

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The role of the liver and the endocrine pancreas in development of hyperinsulinemia in different types of obesity remains unclear. Sedentary rats (160 g) were fed a low-fat-diet (LFD, chow 13% kcal fat), high-fat-diet (HFD, 35% fat), or HFD+ 30% ethanol+ 30% fructose (HF-EFr, 22% fat). Overnight-fasted rats were culled after one, four or eight weeks. Pancreatic and hepatic mRNAs were isolated for subsequent RT-PCR analysis. After eight weeks, body weights increased three-fold in the LFD group, 2.8-fold in the HFD group, and 2.4-fold in the HF-EFr (p < 0.01). HF-EFr-fed rats had the greatest liver weights and consumed less food during Weeks 4–8 (p < 0.05). Hepatic-triglyceride content increased progressively in all groups. At Week 8, HOMA-IR values, fasting serum glucose, C-peptide, and triglycerides levels were significantly increased in LFD-fed rats compared to that at earlier time points. The greatest plasma levels of glucose, triglycerides and leptin were observed in the HF-EFr at Week 8. Gene expression of pancreatic-insulin was significantly greater in the HFD and HF-EFr groups versus the LFD. Nevertheless, insulin: C-peptide ratios and HOMA-IR values were substantially higher in HF-EFr. Hepatic gene-expression of insulin-receptor-substrate-1/2 was downregulated in the HF-EFr. The expression of phospho-ERK-1/2 and inflammatory-mediators were greatest in the HF-EFr-fed rats. Chronic intake of both LFD and HFD induced obesity, MetS, and intrahepatic-fat accumulation. The hyperinsulinemia is the strongest in rats with the lowest body weights, but having the highest liver weights. This accompanies the strongest increase of pancreatic insulin production and the maximal decrease of hepatic insulin signaling, which is possibly secondary to hepatic fat deposition, inflammation and other factors.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 94%

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Insulin Production and Resistance in Different Models of Diet-Induced Obesity and Metabolic Syndrome

Alwahsh

Dwyer

Forbes

et al. 2017

IJMS

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“…Reasons for these contradictory findings have not yet been fully understood; however, so far, in most of the studies participants were not stratified according to their consumption of fermented and distilled alcoholic drinks. Indeed, results of studies in patients suffering from liver cirrhosis consuming alcohol but also animal studies using high concentrations of alcohol (6.5 g EtOH/kg/bw) suggest that the kind of alcoholic drink might be critically affecting the progression of liver disease [10][11][12]. For instance, it has been shown that secondary plant compounds such as xanthohumol and isoα-acids found in hop or resveratrol found in grapes at least in experimental settings may beneficially affect the development of liver diseases of various etiologies including NAFLD [13][14][15].…”

Section: Introductionmentioning

confidence: 99%

Moderate consumption of fermented alcoholic beverages diminishes diet-induced non-alcoholic fatty liver disease through mechanisms involving hepatic adiponectin signaling in mice

et al. 2019

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Purpose Results of some epidemiological studies suggest that moderate alcohol consumption may be associated with a decreased risk to develop NAFLD. Here, the effect of the consumption of moderate beer and diluted ethanol, respectively, on the development of NAFLD were assessed. Methods Female C57BL/6J mice were fed a control diet (C-D) or a diet rich in fructose, fat and cholesterol (FFC) enriched isocalorically and isoalcoholically with beer (FFC + B) or plain ethanol (FFC + E) (2.5 g ethanol/kg body weight/day) for 7 weeks. Liver damage was assessed by histology using NAFLD activity score. Markers of inflammation, insulin resistance and adiponectin signaling were measured at mRNA and protein levels. Using J774A.1 cells as a model of Kupffer cells, the effect of alcoholic beverages on adiponectin receptor 1 (Adipor1) was assessed. Results Hepatic triglyceride concentration, neutrophil granulocytes, iNOS protein concentrations and early signs of insulin resistance found in FFC-fed mice were significantly attenuated in FFC+ B-fed mice (P < 0.05 for all). These findings were associated with a super-induction of Adipor1 mRNA expression (+ ~ 18-fold compared to all other groups) and a decrease of markers of lipid peroxidation in liver tissue of FFC + B-fed mice when compared to FFC-fed animals. Similar differences were not found between FFC-and FFC+ E-fed mice. Expression of Adipor1 was also super-induced (7.5-fold) in J774A.1 cells treated with beer (equivalent to 2 mmol/L ethanol). Conclusions These data suggest that moderate intake of fermented alcoholic beverages such as beer at least partially attenuates NAFLD development through mechanisms associated with hepatic AdipoR1 expression.

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“…For example, resveratrol, a polyphenolic compound notably presented in red wine, has been reported to prevent hepatic steatosis and endoplasmic reticulum stress induced by long‐term high‐fat diet . The hops in beer markedly attenuated acute alcohol‐induced liver steatosis . Er Guo Tou (EGT) is a very common and popular Chinese spirit, especially in the northeast and north of China.…”

Section: Introductionmentioning

confidence: 99%

Chronic moderate alcohol consumption relieves high‐fat high‐cholesterol diet‐induced liver fibrosis in a rat model

Sun

Zhuang

Zhang

et al. 2018

Clin Exp Pharma Physio

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Nonalcoholic fatty liver disease is a worldwide health issue and chronic alcohol consumption may have different effects on this disease. This study explored the role of chronic moderate alcohol consumption on high-fat high-cholesterol (HFHC) diet-induced liver fibrosis in a rodent model. Male Sprague-Dawley rats were divided into five groups: standard chow group, standard chow plus Er Guo Tou (EGT, a Chinese spirit made from fermented cereals) group, HFHC group, HFHC plus EGT group, and HFHC plus pure ethanol (EtOH) group. Rats were fed standard chow or HFHC chow for 12 weeks. EGT or pure ethanol was administrated at a daily dose of 4 g/kg body weight via intra-gastric gavage from week 4. At the end of week 12, hematoxylin and eosin staining, Sirius red and immunohistochemistry of liver sections were examined. The hepatic expression of F4/80, TNF-α, IL-1β, IL-6, CXCL1, CXCL2, α-SMA, Collagen, TGF-β, MMP2, MMP9, and TIMP1 was calculated. Both moderate EGT and pure ethanol did not increase plasma endotoxin in the portal vein comparing with the FHFC group. EGT and pure ethanol did not improve hepatic inflammation, but ameliorated liver fibrosis in histology. Moderate EGT and pure ethanol ameliorated HFHC diet-induced activation of Kupffer cells and hepatic stellate cells. In conclusion, chronic moderate EGT and pure ethanol could ameliorate HFHC diet-induced liver fibrosis.

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Beer Is Less Harmful for the Liver than Plain Ethanol: Studies in Male Mice Using a Binge-Drinking Model

Abstract: Our data suggest that beer is less harmful on the development of acute alcohol-induced liver damage than plain ethanol in male mice.

Cited by 15 publications

References 22 publications

Insulin Production and Resistance in Different Models of Diet-Induced Obesity and Metabolic Syndrome

Insulin Production and Resistance in Different Models of Diet-Induced Obesity and Metabolic Syndrome

Moderate consumption of fermented alcoholic beverages diminishes diet-induced non-alcoholic fatty liver disease through mechanisms involving hepatic adiponectin signaling in mice

Chronic moderate alcohol consumption relieves high‐fat high‐cholesterol diet‐induced liver fibrosis in a rat model

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