The effects of low dietary levels of polyunsaturates on alcohol-induced liver disease in Rhesus monkeys

Pawlosky, Robert J.; Flynn, Bridget; Salem, Norman

doi:10.1002/hep.510260602

Cited by 42 publications

(20 citation statements)

References 30 publications

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“…The results of present study were consistent with previous studies [11, 26, 27], and compositions of total n-3 PUFA, n-6 PUFA, and C20:5n-3 + C22:6n-3 decreased in alcohol group compared with WC group. However, the effect of alcohol on plasma and kidney fatty acids was less evident compared with changes of hepatic fatty acid composition, while TFL could even significantly increase kidney n-6 PUFA and total PUFA content compared with EC.…”

Section: Discussionsupporting

confidence: 93%

“…Although the alcohol consumption of SD rats in the present study was relatively low (from 2.4 to 2.7 g/d/kg body weight), it was demonstrated that chronic periods of moderate alcohol consumption (from 1.2 to 2.6 g/d/kg body weight) were sufficient to decrease PUFA contents of liver [11, 26, 27]. The results of present study were consistent with previous studies [11, 26, 27], and compositions of total n-3 PUFA, n-6 PUFA, and C20:5n-3 + C22:6n-3 decreased in alcohol group compared with WC group.…”

Section: Discussionmentioning

confidence: 82%

“…However, the effect of alcohol on plasma and kidney fatty acids was less evident compared with changes of hepatic fatty acid composition, while TFL could even significantly increase kidney n-6 PUFA and total PUFA content compared with EC. It might be due to that ethanol is mainly metabolized in the liver and ethanol metabolism is capable of generating reactive oxygen species (ROS), which mainly react with PUFA in the liver [11, 28]. In contrast, red wine was reported to preserve kidney long-chain PUFA and nonalcoholic components were reported to contribute to the result [9, 10].…”

Section: Discussionmentioning

confidence: 99%

“…Red wine is supposed to exert an evident protective effect on cardiovascular system, and nonalcoholic components, such as polyphenols in the red wine, might play a significant role in its protection effects [5–7]. In addition, alcohol could decrease tissue polyunsaturated fatty acids (PUFA) including C20:4n-6 and C22:6n-3 in animal studies [8–11], while this decrease could be attenuated or even reversed by red wine consumption, which might be attributed to the effects of nonalcoholic components [9, 10]. Chinese liquor contains abundant nonalcoholic components [12] and is consumed widely around China.…”

Section: Introductionmentioning

confidence: 99%

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Consumption of Chinese Tea‐Flavor Liquor Improves Circulating Insulin Levels without Affecting Hepatic Lipid Metabolism‐Related Gene Expression in Sprague‐Dawley Rats

Zheng

Chen

et al. 2013

The Scientific World Journal

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Objective. To examine the effect of two Chinese liquors with quite different nonalcoholic components on insulin sensitivity, tissue polyunsaturated fatty acids (PUFA), and hepatic lipid metabolism in SD rats. Methods. Thirty-three SD rats were randomized into four groups and maintained in each treatment for 10 weeks: Chinese tea-flavor liquor (TFL, n = 9), traditional Chinese liquor (TCL, n = 8), ethanol control (EC, n = 8), and water control (WC, n = 8). Results. TFL significantly decreased plasma insulin (P = 0.009) and marginally decreased Homeostatic Model Assessment-Insulin Resistance (HOMA-IR) (P = 0.05), compared with WC. Hepatic total and n-6 PUFA compositions were significantly decreased in TFL, TCL, and EC groups compared with WC group (P < 0.05). TFL significantly increased kidney n-6 PUFA (P = 0.05) and total PUFA (P = 0.039), compared with EC group. EC group showed significant higher gene expressions of acetyl-CoA carboxylase and steroid response element-binding protein (1c and 2), while there were no significant differences of these gene expressions in TFL or TCL group compared with WC. Conclusions. TFL has a beneficial effect on metabolic disorder in relation to improved circulating insulin levels without affecting hepatic lipid metabolism-related gene expressions in rats.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 82%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Consumption of Chinese Tea‐Flavor Liquor Improves Circulating Insulin Levels without Affecting Hepatic Lipid Metabolism‐Related Gene Expression in Sprague‐Dawley Rats

Zheng

Chen

et al. 2013

The Scientific World Journal

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“…For instance, we have recently demonstrated a beneficial effect of a diet containing polyunsaturated fatty acids (PUFA) with physiological levels of arachidonic and docosahexaenoic acids on effectively preventing protein oxidation, mitochondrial dysfunction, and ultimately alcoholic fatty liver [137]. These results observed in rats are consistent with the beneficial effects of PUFA diets against alcoholic fatty liver in monkeys [138] and nonalcoholic fatty liver in rats fed a choline-deficient high fat diet [139]. Our results also provide the underlying mechanisms by which physiologically relevant levels of PUFA exert beneficial effects against alcoholic fatty liver in both rats [137] and monkeys [138].…”

Section: Potential Translational Applications Of Redox Proteomics mentioning

confidence: 67%

Increased Nitroxidative Stress Promotes Mitochondrial Dysfunction in Alcoholic and Nonalcoholic Fatty Liver Disease

Song

Abdelmegeed

Henderson

et al. 2013

Oxidative Medicine and Cellular Longevity

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Increased nitroxidative stress causes mitochondrial dysfunctions through oxidative modifications of mitochondrial DNA, lipids, and proteins. Persistent mitochondrial dysfunction sensitizes the target cells/organs to other pathological risk factors and thus ultimately contributes to the development of more severe disease states in alcoholic and nonalcoholic fatty liver disease. The incidences of nonalcoholic fatty liver disease continuously increase due to high prevalence of metabolic syndrome including hyperlipidemia, hypercholesterolemia, obesity, insulin resistance, and diabetes. Many mitochondrial proteins including the enzymes involved in fat oxidation and energy supply could be oxidatively modified (including S-nitrosylation/nitration) under increased nitroxidative stress and thus inactivated, leading to increased fat accumulation and ATP depletion. To demonstrate the underlying mechanism(s) of mitochondrial dysfunction, we employed a redox proteomics approach using biotin-N-maleimide (biotin-NM) as a sensitive biotin-switch probe to identify oxidized Cys residues of mitochondrial proteins in the experimental models of alcoholic and acute liver disease. The aims of this paper are to briefly describe the mechanisms, functional consequences, and detection methods of mitochondrial dysfunction. We also describe advantages and limitations of the Cys-targeted redox proteomics method with alternative approaches. Finally, we discuss various applications of this method in studying oxidatively modified mitochondrial proteins in extrahepatic tissues or different subcellular organelles and translational research.

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Inactivation of oxidized andS-nitrosylated mitochondrial proteins in alcoholic fatty liver of rats

et al. 2006

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Increased oxidative/nitrosative stress is a major contributing factor to alcohol-mediated mitochondrial dysfunction. However, which mitochondrial proteins are oxidatively modified under alcohol-induced oxidative/nitrosative stress is poorly understood. The aim of this study was to systematically investigate oxidized and/or S-nitrosylated mitochondrial proteins and to use a biotin-N-maleimide probe to evaluate their inactivation in alcoholic fatty livers of rats. Binge or chronic alcohol exposure significantly elevated nitric oxide, inducible nitric oxide synthase, and ethanol-inducible CYP2E1. The biotin-N-maleimide-labeled oxidized and/or S-nitrosylated mitochondrial proteins from pair-fed controls or alcohol-fed rat livers were subsequently purified with streptavidin-agarose. The overall patterns of oxidized and/or S-nitrosylated proteins resolved by 2-dimensional polyacrylamide gel electrophoresis were very similar in the chronic and binge alcohol treatment groups. Seventy-nine proteins that displayed differential spot intensities from those of control rats were identified by mass spectrometry. These include mitochondrial aldehyde dehydrogenase 2 (ALDH2), ATP synthase, acyl-CoA dehydrogenase, 3-ketoacyl-CoA thiolase, and many proteins involved in chaperone activity, mitochondrial electron transfer, and ion transport. The activity of 3-ketoacyl-CoA thiolase involved in mitochondrial ␤-oxidation of fatty acids was significantly inhibited in alcohol-exposed rat livers, consistent with hepatic fat accumulation, as determined by biochemical and histological analyses. Measurement of activity and immunoblot results showed that ALDH2 and ATP synthase were also inhibited through oxidative modification of their cysteine or tyrosine residues in alcoholic fatty livers of rats. In conclusion, our results help to explain the underlying mechanism for mitochondrial dysfunction and increased susceptibility to alcohol-mediated liver damage. Supplementary material for this article can be found on the HEPATOLOGY website (http://interscience.wiley.com/jpages/0270-9139/suppmat/index.html).

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The effects of low dietary levels of polyunsaturates on alcohol-induced liver disease in Rhesus monkeys

Cited by 42 publications

References 30 publications

Consumption of Chinese Tea‐Flavor Liquor Improves Circulating Insulin Levels without Affecting Hepatic Lipid Metabolism‐Related Gene Expression in Sprague‐Dawley Rats

Consumption of Chinese Tea‐Flavor Liquor Improves Circulating Insulin Levels without Affecting Hepatic Lipid Metabolism‐Related Gene Expression in Sprague‐Dawley Rats

Increased Nitroxidative Stress Promotes Mitochondrial Dysfunction in Alcoholic and Nonalcoholic Fatty Liver Disease

Inactivation of oxidized andS-nitrosylated mitochondrial proteins in alcoholic fatty liver of rats

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