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• W2053313128 abstract "It is now generally agreed that alcohol abuse, rather than the accompanying malnutrition, is the primary cause of alcoholic liver disease.1Medical and nutritional complications of alcoholism: mechanisms and management. Plenum Press:, New York1992Google Scholar, 2Lieber CS DeCarli LM Rubin E. Sequential production of fatty liver, hepatitis, and cirrhosis in sub-human primates fed ethanol with adequate diets.Proc Natl Acad Sci USA. 1975; 72: 437-441Google Scholar This is a departure from earlier views based on rodent studies.3Best CH Hartroft WS Lucas CC Ridout OH. Liver damage produced by feeding alcohol or sugar and its prevention by choline.Br Med J. 1949; 2: 1001Google Scholar Nevertheless, it is also becoming apparent that nutritional factors may modify the development and subsequent course of alcohol-induced hepatic injury. A number of experimental and clinical data bear on this. First, increased fat intake appears to worsen the severity of fat deposition in the liver when combined with ethanol.4Lieber CS DeCarli LM. Quantitative relationship between amount of dietary fat and severity of alcoholic fatty liver.Am J Clin Nutr. 1970; 23: 474-478Google Scholar, 5Lieber CS Spritz N. Effects of prolonged ethanol intake in man: role of dietary, adipose and endogenously synthesized fatty acids in the pathogenesis of alcoholic fatty liver.J Clin Invest. 1966; 45: 1400-1411Google Scholar Second, some forms of unsaturated fat potentiate alcohol-induced liver damage, apparently by serving as substrate for the formation of reactive free radicals and eicosanoids.6Nanji AA French SW. Dietary linoleic acid is required for development of experimentally induced alcoholic liver injury.Life Sci. 1989; 44: 223-227Google Scholar, 7Nanji AA Zhao S Dannenberg AJ Sadrzadek SMH Waxman DJ. Changes in cytochromes P450, 2E1, 2B, and 4A and phospholipases A and C in the intragastric feeding rat model for alcoholic liver disease: relationship to dietary fats and pathologic liver injury.Alcohol Clin Exp Res. 1994; 18: 902-908Google Scholar, 8Mezey E. Dietary fat and alcoholic liver disease.Hepatology. 1998; 28: 901-905Google Scholar Third, an apparent increase in iron absorption and its accumulation in the liver of alcoholic patients may enhance hepatic damage by greater lipid peroxidation.9Chapman RW Morgan MY Laulicht M Hoffbrand AV Sherlock S. Hepatic iron stores and markers of iron overload in alcoholics and patients with idiopathic hemochromatosis.Dig Dis Sci. 1982; 27: 909-916Google Scholar, 10Bacon BR Britton RS. The pathology of hepatic iron overload: a free radical-mediated process.Hepatology. 1990; 11: 127-137Google Scholar, 11Tsukamoto H Horne W Kamimura S Niemela O Pakkila S Yia-Herttuala S et al.Experimental liver cirrhosis induced by alcohol and iron.J Clin Invest. 1995; 96: 620-630Google Scholar Fourth, malnutrition is common in many patients with alcoholic liver disease, and the severity of the malnutrition and extent of hepatic dysfunction correlate, although not necessarily as a cause and effect.12Schenker S Halff GA. Nutritional therapy in alcoholic liver disease.Semin Liver Dis. 1993; 13: 196-209Google Scholar, 13Mendenhall CL Anderson S Weesner RE Goldberg SJ Crolic KA. Protein calorie malnutrition associated with alcoholic hepatitis.Am J Med. 1984; 76: 211-222Google Scholar Finally, and perhaps most important clinically, there is now good evidence that some important nutrients—that is, S-adenosyl-L -methionine, polyenylphosphatidylcholine, and glutathione (especially in mitochondria)—may be depleted in patients with alcohol abuse or alcoholic liver disease.14Osman E Owens JS Burroughs AK. Review article: S-Adensylmethionine: a new therapeutic agent in liver disease.Aliment Pharmacol Ther. 1993; 7: 21-28Google Scholar, 15Lieber CS Robins SJ Leo MA. Hepatic phosphatidylethanolamine methyltransferase activity is decreased by ethanol and increased by phosphatidylcholine.Alcohol Clin Exp Res. 1994; 18: 592-595Google Scholar, 16Colell A Garcia-Ruiz C Miranda M Ardite E Mari M Morales A et al.Selective glutathione depletion of mitochondria by ethanol sensitizes hepatocytes to tumor necrosis factor.Gastroenterology. 1998; 115: 1541-1551Google Scholar, 17Fernandez-Checa JC Kaplowitz N Garcia-Ruiz C Colell A. Mitochondria glutathione: importance and transport.Semin Liver Dis. 1998; 18: 389-402Google Scholar These considerations have prompted investigations into the possible therapeutic benefits of replenishing or modifying some of the altered nutrients in patients with alcoholic liver disease. The study by Oneta et al in this issue of the Journal18Oneta CM Mak KM Lieber CS. Dilinoleoylphosphatidylcholine selectively modulates lipopolysaccharide-induced Kupffer cell activation.J Lab Clin Med. 1999; 134: 466-470Google Scholar is one of a series of important articles from this group concerning this nutritional supplement. Another major incentive for such studies has been research progress in identifying the cellular mechanisms that are deranged in various sequential stages of alcoholic liver disease (fat accumulation, necrosis, inflammation, and fibrosis).19Bradham CA Plumpa J Manns MP Brenner DA Trautwein C. Mechanisms of hepatic toxicity. I. TNF-induced liver injury.Am J Physiol. 1998; 275: G387-G392Google Scholar, 20Colell A Garcia-Ruiz C Miranda M Ardite E Mari M Morales A et al.Selective glutathione depletion of mitochondria by ethanol sensitizes hepatocytes to tumor necrosis factor.Gastroenterology. 1998; 115: 1541-1551Google Scholar, 21Iimuro Y Gallucci RM Luster MI Kono H Thurman RG. Antibodies to tumor necrosis factor alfa attenuate hepatic necrosis and inflammation caused by chronic exposure to ethanol in the rat.Hepatology. 1997; 26: 1530-1537Google Scholar, 22Maher JJ Friedman SL. Pathogenesis of hepatic fibrosis.in: Hall P Alcoholic liver disease: pathology and pathogenesis.2nd ed. Edward Arnold, London1995: 71-88Google Scholar, 23Olaso E Friedman SL. Molecular regulation of hepatic fibrogenesis.J Hepatol. 1998; 29: 836-847Google Scholar This has permitted the testing of various substances (including nutrients) on the function of specific hepatic cells and their dysfunction (ie, sensitivity to endotoxin, cytokine release, and altered signaling) after exposure to alcohol. Before considering specifically the article on the possible effects of DLPC on Kupffer cells,18Oneta CM Mak KM Lieber CS. Dilinoleoylphosphatidylcholine selectively modulates lipopolysaccharide-induced Kupffer cell activation.J Lab Clin Med. 1999; 134: 466-470Google Scholar it is worthwhile to orient the readers as to the present concepts of the mechanisms of alcohol-induced liver damage. As shown in very simplified form in Fig 1, alcoholic liver injury is felt to have a multifactorial basis.Key primary factors are felt to be alcohol-enhanced effects of gut bacterial endotoxin and oxidative stress on liver macrophages (Kupffer cells). The activation of Kupffer cells may be caused by greater permeability of the gut to endotoxin24Bjarnason I Ward K Peters TJ. The leaky gut of alcoholism: possible route of entry for toxic compounds.Lancet. 1984; 1: 179-182Google Scholar (an effect accentuated by estrogen25Enomoto N Schemmer P Rivera CA Bradford BU Enomoto A Brenner DA et al.Estriol sensitizes rat Kupffer cells by increasing permeability to gut-derived endotoxin.Gastroenterology. 1999; 116: A1207Google Scholar) and its increased binding to endotoxin receptors in Kupffer cells chronically exposed to ethanol.26Enomoto N Ikejima K Bradford B Rivera C Kono H Brenner DA et al.Alcohol causes both tolerance and sensitization of rat Kupffer cells via mechanisms dependent on endotoxin.Gastroenterology. 1998; 115: 443-451Google Scholar Activated Kupffer cells, in turn, promote the release of a cascade of cytokines (likely via control of the transcription factor NF-κB) influencing inflammation/necrosis/apoptosis and fibrosis (Fig 1). Alcohol/acetaldehyde effects on mitochondria, sensitized to tumor necrosis factor TNF-α via selective glutathione depletion and the role of acetaldehyde adducts per se, or via an immune effect, may well also contribute to this pleiomorphic effect of alcohol abuse. The relative importance of these pathways and effects, not all of which are shown in Fig 1, is not certain. Nevertheless, the central role of the Kupffer cells has been well documented in experimental studies (reviewed in reference 27Schenker S Bay M. Alcohol and endotoxin: another path to alcoholic liver injury?.Alcohol Clin Exp Res. 1995; 19: 1364-1366Google Scholar); hence the studies of the effect of DLPC on these cells, reported here,18Oneta CM Mak KM Lieber CS. Dilinoleoylphosphatidylcholine selectively modulates lipopolysaccharide-induced Kupffer cell activation.J Lab Clin Med. 1999; 134: 466-470Google Scholar have focused on an appropriate cell. How did the study of DLPC evolve? It began logically with the findings that in animals exposed to chronic ethanol, there was a decrease in hepatic phosphatidylethanolamine methyl transferase activity and in the appropriate phospholipids.15Lieber CS Robins SJ Leo MA. Hepatic phosphatidylethanolamine methyltransferase activity is decreased by ethanol and increased by phosphatidylcholine.Alcohol Clin Exp Res. 1994; 18: 592-595Google Scholar This led to studies of baboons with alcohol-induced hepatic fibrosis given PPC (a mixture of polyunsaturated phospholipids extracted from soybeans) in a controlled setting.28Lieber CS Robins SJ Li J De Carli LM Mak K Fasulo JM et al.Phosphatidylcholine protects against fibrosis and cirrhosis in the baboon.Gastroenterology. 1994; 106: 152-159Google Scholar, 29Lieber CS Casini A DeCarli LM Mak KM Kim CI Leo MA. Attenuation of alcohol-induced hepatic fibrosis by polyunsaturated lecithin.Hepatology. 1990; 12: 1390-1398Google Scholar The use of PPC clearly showed a decrease in hepatic fibrosis and an increase in hepatic phosphatidyl ethanolamine methyl transferase in the baboons.28Lieber CS Robins SJ Li J De Carli LM Mak K Fasulo JM et al.Phosphatidylcholine protects against fibrosis and cirrhosis in the baboon.Gastroenterology. 1994; 106: 152-159Google Scholar, 29Lieber CS Casini A DeCarli LM Mak KM Kim CI Leo MA. Attenuation of alcohol-induced hepatic fibrosis by polyunsaturated lecithin.Hepatology. 1990; 12: 1390-1398Google Scholar A similar protective effect of PPC was shown in rats with other forms of hepatic fibrosis.30Ma X Zhao J Lieber CS. Polyenylphosphatidylcholine attenuates non-alcoholic hepatic fibrosis and accelerates its regression.J Hepatol. 1996; 24: 604-613Google Scholar These encouraging experimental findings are now being assessed for patient relevance in a multicenter Veterans Administration study. Assuming their applicability to patients, a key question is the mechanism involved. As shown in Table I, a series of possible beneficial effects of PPC on various aspects of hepatic function have been reported by Dr C. S. Lieber and his associates.Table IPossible mechanisms of action of polyenylphosphatidylcholine on the liver1. Enhanced collagenase activity30Ma X Zhao J Lieber CS. Polyenylphosphatidylcholine attenuates non-alcoholic hepatic fibrosis and accelerates its regression.J Hepatol. 1996; 24: 604-613Google Scholar2. Decrease in hepatic fat accumulation and improved mitchondrial function31Navder KP Baraona E Lieber CS. Polyenylphosphatidylcholine attenuates alcohol-induced fatty liver and hyperlipemia in rats.J Nutr. 1997; 127: 1800-1806Google Scholar3. Decrease in oxidative stress32Lieber CS Leo MA Aleynik SI Aleynik MK DeCarli LM. Polyenylphosphatidylcholine decreases alcohol-induced oxidative stress in the baboon.Alcohol Clin Exp Res. 1997; 21: 375-379Google Scholar, 33Aleynik SI Leo MA Ma X Aleynik MK Lieber CS. Polyenylphosphotidylcholine prevents carbon tetracholoride-induced lipid peroxidation while it attenuates liver fibrosis.J Hepatol. 1997; 27: 554-561Google Scholar4. Decrease in hepatic stellate cell activation (decrease in fibrosis)34Poniachik J Baraona E Zhao J Lieber CS. Dilinoleoylphosphatidylcholine decreases hepatic stellate cell activation.J Lab Clin Med. 1999; 133: 342-348Google Scholar5. Decreased activation of Kupffer cells by endotoxin withaltered cytokine profile “release”18Oneta CM Mak KM Lieber CS. Dilinoleoylphosphatidylcholine selectively modulates lipopolysaccharide-induced Kupffer cell activation.J Lab Clin Med. 1999; 134: 466-470Google Scholar Open table in a new tab It is evident that the protective effects of PPC could be exerted at many levels of cellular function and signaling. The latest observations18Oneta CM Mak KM Lieber CS. Dilinoleoylphosphatidylcholine selectively modulates lipopolysaccharide-induced Kupffer cell activation.J Lab Clin Med. 1999; 134: 466-470Google Scholar of an effect of this nutrient on Kupffer cells (a key cell in this cascade) and on TNF-α, a key cytokine,21Iimuro Y Gallucci RM Luster MI Kono H Thurman RG. Antibodies to tumor necrosis factor alfa attenuate hepatic necrosis and inflammation caused by chronic exposure to ethanol in the rat.Hepatology. 1997; 26: 1530-1537Google Scholar, 35Taub R Blocking NF-κB in the liver: the good and bad news.Hepatology. 1998; 28: 1445-1446Google Scholar, 36Xu Y Czaja MJ Bessin M Glutathione (GSH) depletion sensitizes liver cells to TNF-α cytotoxicity [abstract].Hepatology. 1996; 24: 186AGoogle Scholar are conceptually especially important. In addition, the current study has defined the specificity of the PPC lipid component by showing that it is the DLPC and not other phosphatidylcholines that exert the protective effect.18Oneta CM Mak KM Lieber CS. Dilinoleoylphosphatidylcholine selectively modulates lipopolysaccharide-induced Kupffer cell activation.J Lab Clin Med. 1999; 134: 466-470Google Scholar It is, of course, essential to point out a number of caveats. First, some of these mechanistic studies, including the current one,18Oneta CM Mak KM Lieber CS. Dilinoleoylphosphatidylcholine selectively modulates lipopolysaccharide-induced Kupffer cell activation.J Lab Clin Med. 1999; 134: 466-470Google Scholar have been carried out in vitro, with isolated cells, at a given concentration of DLPC, and in the absence of ethanol. In view of the complexity of the in vivo intercell signaling (Fig 1),37Jones BE Czaja MJ. Mechanisms of hepatic toxicity. III. Intracellular signaling in response to toxic liver injury.Am J Physiol. 1998; 275: G874-G878Google Scholar the many effects of TNF-α,35Taub R Blocking NF-κB in the liver: the good and bad news.Hepatology. 1998; 28: 1445-1446Google Scholar, 38Naismith JH Sprang SR. Modularity in the TNF-receptor family.Trends Biochem Sci. 1998; 23: 74-79Google Scholar, 39Baker SJ Reddy EP. Transducers of life and death: TNF receptor superfamily and associated proteins.Oncogene. 1996; 12: 1-9Google Scholar and likely other cytokines, and the various effects of ethanol, these studies admittedly need to be verified in experimental animals in vivo. Second, the concentration of DLPC used is consistent with that used in prior collagenase studies40Lieber CS Robins SJ Li J DeCarli LM Mak KM Fasulo JM et al.Phosphatidylcholine protects against fibrosis and cirrhosis in the baboon.Gastroenterology. 1994; 106: 152-159Google Scholar and is in the range of values seen in patients given this supplement (C. S. Lieber, personnal communication). Other doses of the supplement, however, will need to be assessed, and a dose- and time-response curve of various concentrations of DLPC on cell function in vitro will be of interest. This is because it is not certain whether the reported degree of opposite change in TNF-α and interleukin-1β,18Oneta CM Mak KM Lieber CS. Dilinoleoylphosphatidylcholine selectively modulates lipopolysaccharide-induced Kupffer cell activation.J Lab Clin Med. 1999; 134: 466-470Google Scholar although statistically significant, has physiologic (clinical) impact. Perhaps these effects can be enhanced with higher doses (concentrations) of the supplement. Third, it is of interest that DLPC, an unsaturated phospholipid, has an antioxidant effect.32Lieber CS Leo MA Aleynik SI Aleynik MK DeCarli LM. Polyenylphosphatidylcholine decreases alcohol-induced oxidative stress in the baboon.Alcohol Clin Exp Res. 1997; 21: 375-379Google Scholar, 33Aleynik SI Leo MA Ma X Aleynik MK Lieber CS. Polyenylphosphotidylcholine prevents carbon tetracholoride-induced lipid peroxidation while it attenuates liver fibrosis.J Hepatol. 1997; 27: 554-561Google Scholar This is an unexpected finding that requires a mechanistic explanation. It may be, as has been suggested,32Lieber CS Leo MA Aleynik SI Aleynik MK DeCarli LM. Polyenylphosphatidylcholine decreases alcohol-induced oxidative stress in the baboon.Alcohol Clin Exp Res. 1997; 21: 375-379Google Scholar that various polyunsaturated fats affect cell membranes differently. DLPC may also decrease oxidative stress by inhibiting free radical generation via cytochrome P4502E1.41Aleynik MK Leo MA Aleynik SJ Lieber CS. Polyenylphosphatidylcholine opposes the increase of cytochrome P450E1 by ethanol and corrects it iron-induced decrease.Alcohol Clin Exp Res. 1999; 23: 96-100Google Scholar Finally, although such experimental studies are essential to dissect mechanisms, eventually one must also address the reasons why only a small percentage (20% to 30%) of alcohol abusers progress to severe liver disease (cirrhosis). Until an animal model of such hepatic sensitivity to alcohol is found, the problem will need to be studied in human patients. Based on the multiple mechanisms of action of DLPC, this nutrient may be beneficial for other forms of chronic liver disease wherein oxidative stress, cytokine alterations, and fibrosis ensue. Given the apparent safety of this agent28Lieber CS Robins SJ Li J De Carli LM Mak K Fasulo JM et al.Phosphatidylcholine protects against fibrosis and cirrhosis in the baboon.Gastroenterology. 1994; 106: 152-159Google Scholar, 29Lieber CS Casini A DeCarli LM Mak KM Kim CI Leo MA. Attenuation of alcohol-induced hepatic fibrosis by polyunsaturated lecithin.Hepatology. 1990; 12: 1390-1398Google Scholar and its acceptable cost, such studies would appear to be worthwhile. Alcoholic liver disease is still a very important clinical problem42Grant BF DeBakey S Zobeck TS. Surveillance report no. 18. Liver cirrhosis mortality in the US 1973-1988. National Institute on Alcohol Abuse and Alcoholism. Division of Biometry and Epidemiology. US Department of Health and Human Services, Rockville, MD1991Google Scholar and is compounded in severity by the co-occurrence of hepatitis C in some 30 percent of such individuals.43Greillier LFL Dusheiko GM. The role of hepatitis C virus in alcoholic liver disease.Alcohol Alcoholism. 1997; 32: 103-111Google Scholar The treatment of alcoholic liver injury, like its pathogenesis, is likely to benefit from a multifactorial approach. This will involve interrupting, or at least modifying, the craving for alcohol,44Volpicelli JR Clay KL Watson NT Volpicelli BA. Naltrexone and the treatment of alcohol dependence.Alcohol Health Res World. 1994; 18: 272-278Google Scholar, 45Davidson D Palfai T Bird C Swift R. Effects of Naltrexone on alcohol self-administration in heavy drinkers.Alcohol Clin Exp Res. 1999; 23: 195-203Google Scholar, 46Schenker S Bay MK. Medical problems associated with alcoholism.in: Advances in internal medicine. vol 43. Mosby-Year Book Inc, Chicago1998: 27-78Google Scholar identifying individuals especially susceptible to severe liver damage,27Schenker S Bay M. Alcohol and endotoxin: another path to alcoholic liver injury?.Alcohol Clin Exp Res. 1995; 19: 1364-1366Google Scholar, 47Schenker S, Martin R. Treatment of alcoholic liver disease. In: Arroyo V, editor. Aspects in the therapy of liver diseases. Barcelona: Masson. In press.Google Scholar and using multiple therapeutic agents (including nutrients) that influence specific biologic/cellular processes altered by alcohol (Fig 1). For instance, the use of S-adenosyl-L -methionine (perhaps together with DLPC), which restores mitochondrial glutathione after alcohol exposure,48Colell A Garcia-Ruiz C Morales A Ballesta A Ookhtens M Rodes J et al.Transport of reduced glutathione in hepatic mitochondrial and mitoplasts from ethanol-treated rats: effect of membrane physical properties and S-adenosyl-L -methionine.Hepatology. 1997; 26: 699-708Google Scholar, 49Gigliozzi A Romeo R Fraioli F Cantafora A Delle Monache M Cardilli A et al.Effect of S-adenosyl-L -methionine and dilinoleoylphosphatidylcholine on liver lipid composition and ethanol hepatotoxicity in isolated perfused rat liver.Dig Dis Sci. 1998; 43: 2211-2222Google Scholar may be an example of such target-selected therapy. The type of focused in vitro study reported in this issue of the Journal18Oneta CM Mak KM Lieber CS. Dilinoleoylphosphatidylcholine selectively modulates lipopolysaccharide-induced Kupffer cell activation.J Lab Clin Med. 1999; 134: 466-470Google Scholar is likely to enhance meaningful therapy based on sound and specific experimental knowledge." @default.
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• W2053313128 title "New concepts of dietary intervention in alcoholic liver disease" @default.
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