Beef Fat Prevents Alcoholic Liver Disease in the Rat

Nanji, Amin A.; Mendenhall, Charles L.; French, Samuel W.

doi:10.1111/j.1530-0277.1989.tb00276.x

Cited by 262 publications

(146 citation statements)

References 17 publications

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“…Histological examination was carried out by a pathologist who had no prior knowledge of the dietary groups. The liver pathology score was calculated as follows 15,16 : steatosis (the percentage of liver cells containing fat): 1ϩ, less than 25% of cells containing fat; 2ϩ, 26% to 50%; 3ϩ, 51% to 75%; and 4ϩ, more than 75%; inflammation and necrosis: one focus/lobule, 1ϩ; two or more foci/lobule, 2ϩ. The total liver pathology score was calculated by adding the scores from each of the parameters.…”

Section: Methodsmentioning

confidence: 99%

“…On the basis of epidemiologic observations relating the type of dietary fat to ALD, 14 studies in the intragastric feeding model have shown that rats fed saturated fat with ethanol develop none of the histologic features of ALD, whereas rats fed polyunsaturated fatty acids (PUFA) with ethanol show fatty liver, necrosis, inflammation, and fibrosis. 15,16 In particular, rats fed fish oil (a very rich source of PUFA) with ethanol develop more severe liver injury than rats fed corn oil and ethanol. 17,18 When palm oil is fed with ethanol, the rats develop only fatty liver with no necrosis or inflammation.…”

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confidence: 99%

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Increased lipid peroxidation and impaired antioxidant enzyme function is associated with pathological liver injury in experimental alcoholic liver disease in rats fed diets high in corn oil and fish oil

et al. 1998

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Increased hepatic oxidative stress with ethanol administration is hypothesized to be caused either by enhanced pro-oxidant production or decreased levels of antioxidants or both. We used the intragastric feeding rat model to assess the relationship between hepatic antioxidant enzymes and pathological liver injury in animals fed different dietary fats. Male Wistar rats (5 per group) were fed ethanol with either medium-chain triglycerides (MCTE), palm oil (PE), corn oil (CE), or fish oil (FE). Control animals were fed isocaloric amounts of dextrose instead of ethanol with the same diets. The following were evaluated in each group: liver pathology, lipid peroxidation, manganese superoxide dismutase (MnSOD) levels, copper-zinc SOD (CuZnSOD) levels, glutathione peroxidase (GPX) levels, and catalase (CAT) levels. All enzymes were evaluated using activity assays and immunoblots. Rats fed FE showed the most severe pathology (fatty liver, necrosis, and inflammation), those fed CE showed moderate changes, those fed PE showed fatty liver only, and those fed MCTE were normal. Parameters indicative of lipid peroxidation (conjugated dienes and thiobarbituric acid-reactive substances) were also greater in rat livers from animals fed the diets high in polyunsaturated fatty acids (CE and FE). CuZnSOD, GPX, and CAT activities showed an inverse correlation (r ‫؍‬ ؊.92, P F .01) with severity of pathological injury, with the lowest levels for both enzymes found in FE-fed rats. Decreased enzyme activity in CE-and FE-fed rats was accompanied by similar decreases in immunoreactive protein. Ethanol administration did not cause significant decreases in enzyme activity in groups that showed no necroinflammatory changes (MCTE and PE). MnSOD activity showed no significant change in any ethanol-fed group. Our results show that decreases in CuZnSOD, GPX, and CAT occur in rats showing pathological liver injury and also having the highest levels of lipid peroxidation. These results suggest that feeding dietary substrates that enhance lipid peroxidation can exacerbate both ethanol-induced oxidative damage as well as necroinflammatory changes. The decrease in activity of antioxidant enzymes observed in animals fed diets high in polyunsaturated fatty acids and ethanol could possibly increase the susceptibility to oxidative damage and further contribute to ethanol-induced liver injury. (HEPATOLOGY 1998;27:1317-1323.)

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Section: Methodsmentioning

confidence: 99%

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confidence: 99%

Increased lipid peroxidation and impaired antioxidant enzyme function is associated with pathological liver injury in experimental alcoholic liver disease in rats fed diets high in corn oil and fish oil

et al. 1998

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“…Liver pathology was scored as described by Nanji et al (26) as follows: steatosis (the percentage of liver cells containing fat): Ͻ25% ϭ 1ϩ; Ͻ50% ϭ 2ϩ; Ͻ75% ϭ 3ϩ; Ͼ75% ϭ 4ϩ; inflammation and necrosis: 1 focus per low-power field ϭ 1ϩ; 2 or more ϭ 2ϩ. One point was given for each grade of severity of histological abnormality and a total score was calculated for each liver.…”

Section: Pathological Evaluationmentioning

confidence: 99%

Reduced Early Alcohol-Induced Liver Injury in CD14-Deficient Mice

Yin

Bradford

Wheeler

et al. 2001

The Journal of Immunology

225

125

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Activation of Kupffer cells by gut-derived endotoxin is associated with alcohol-induced liver injury. Recently, it was shown that CD14-deficient mice are more resistant to endotoxin-induced shock than wild-type controls. Therefore, this study was designed to investigate the role of CD14 receptors in early alcohol-induced liver injury using CD14 knockout and wild-type BALB/c mice in a model of enteral ethanol delivery. Animals were given a high-fat liquid diet continuously with ethanol or isocaloric maltose-dextrin as control for 4 wk. The liver to body weight ratio in wild-type mice (5.8 ± 0.3%) was increased significantly by ethanol (7.3 ± 0.2%) but was not altered by ethanol in CD14-deficient mice. Ethanol elevated serum alanine aminotransferase levels nearly 3-fold in wild-type mice, but not in CD14-deficient mice. Wild-type and knockout mice given the control high-fat diet had normal liver histology, whereas ethanol caused severe liver injury (steatosis, inflammation, and necrosis; pathology score = 3.8 ± 0.4). In contrast, CD14-deficient mice given ethanol showed minimal hepatic changes (score = 1.6 ± 0.3, p < 0.05). Additionally, NF-κB, TGF-β, and TNF-α were increased significantly in wild-type mice fed ethanol but not in the CD14 knockout. Thus, chronic ethanol feeding caused more severe liver injury in wild-type than CD14 knockouts, supporting the hypothesis that endotoxin acting via CD14 plays a major role in the development of early alcohol-induced liver injury.

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“…19,20 In this model, we and other investigators have shown that an inverse relationship exists between the saturation of lipids in the diet and the severity of alcohol-induced liver injury. [21][22][23][24] Rats fed ethanol and diets enriched in saturated fatty acids are protected from liver injury, whereas diets enriched in polyunsaturated fatty acids promote alcoholic liver injury. Thus, the rat intragastric feeding model, in which ethanol is fed with different dietary fats, is useful to elucidate the pathogenesis of alcoholic liver disease.…”

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confidence: 99%