Light, but not heavy alcohol drinking, stimulates paraoxonase by upregulating liver mRNA in rats and humans
Paraoxonase 1 (PON) may contribute to the cardioprotective action of high-density lipoprotein (HDL) because it inhibits low-density lipoprotein (LDL) oxidation, a prerequisite for the onset of atherosclerosis. Because light drinking and heavy drinking have diametrically opposite effects on cardiopro...
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| Veröffentlicht in: | Metabolism, clinical and experimental clinical and experimental, 2003-10, Vol.52 (10), p.1287-1294 |
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| container_title | Metabolism, clinical and experimental |
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| creator | Rao, Manjunath N Marmillot, Philippe Gong, Maokaı̈ Palmer, David A Seeff, Leonard B Strader, Doris B Lakshman, M.Raj |
| description | Paraoxonase 1 (PON) may contribute to the cardioprotective action of high-density lipoprotein (HDL) because it inhibits low-density lipoprotein (LDL) oxidation, a prerequisite for the onset of atherosclerosis. Because light drinking and heavy drinking have diametrically opposite effects on cardioprotection, we have determined the effects of ethanol dosage on rat serum PON activity and its hepatic expression. Furthermore, we have investigated PON activity and polymorphism in human light and heavy drinkers. Our results confirm that HDL-PON inhibited LDL oxidation, destroyed oxidized LDL, and inhibited its uptake by macrophages. Light ethanol feeding caused a 20% to 25% (
P < .05) increase in PON activity in both serum and liver and a 59% (
P < .001) increase in the level of liver PON mRNA compared with pair-fed control rats. In contrast, heavy ethanol feeding caused a 25% (
P < .05) decrease in serum and liver PON activities with a 51% (
P < .01) decrease in liver PON mRNA level. Light drinkers had a 395% (
P < .001) higher, whereas heavy drinkers had a 45% (
P < .001) lower serum PON activity compared with nondrinkers. Significantly, the number of homozygotes versus heterozygotes with respect to high or low activity PON phenotype was similar in all the groups. Therefore, we conclude that light drinking upregulates, whereas heavy drinking downregulates PON activity and its expression, irrespective of its genetic polymorphism. |
| doi_str_mv | 10.1016/S0026-0495(03)00191-4 |
| format | Article |
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P < .05) increase in PON activity in both serum and liver and a 59% (
P < .001) increase in the level of liver PON mRNA compared with pair-fed control rats. In contrast, heavy ethanol feeding caused a 25% (
P < .05) decrease in serum and liver PON activities with a 51% (
P < .01) decrease in liver PON mRNA level. Light drinkers had a 395% (
P < .001) higher, whereas heavy drinkers had a 45% (
P < .001) lower serum PON activity compared with nondrinkers. Significantly, the number of homozygotes versus heterozygotes with respect to high or low activity PON phenotype was similar in all the groups. Therefore, we conclude that light drinking upregulates, whereas heavy drinking downregulates PON activity and its expression, irrespective of its genetic polymorphism.]]></description><identifier>ISSN: 0026-0495</identifier><identifier>EISSN: 1532-8600</identifier><identifier>DOI: 10.1016/S0026-0495(03)00191-4</identifier><identifier>PMID: 14564680</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Adult ; Alcohol Drinking - blood ; Alcohol Drinking - metabolism ; Alcoholism and acute alcohol poisoning ; Animals ; Aryldialkylphosphatase ; Biological and medical sciences ; Cardiotonic Agents - administration & dosage ; Cardiotonic Agents - pharmacology ; Down-Regulation - drug effects ; Esterases - blood ; Esterases - genetics ; Esterases - metabolism ; Ethanol - administration & dosage ; Ethanol - pharmacology ; General aspects ; Heterozygote ; Homozygote ; Humans ; Lipoproteins, LDL - metabolism ; Liver - enzymology ; Male ; Medical sciences ; Middle Aged ; Oxidation-Reduction - drug effects ; Polymorphism, Genetic ; Rats ; Rats, Wistar ; RNA, Messenger - metabolism ; Toxicology</subject><ispartof>Metabolism, clinical and experimental, 2003-10, Vol.52 (10), p.1287-1294</ispartof><rights>2003 Elsevier Inc.</rights><rights>2004 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c391t-aa76ef0caa64e3eeb6cb6374d614a0ae94461fdcca090b348cd5e0c963c666dc3</citedby><cites>FETCH-LOGICAL-c391t-aa76ef0caa64e3eeb6cb6374d614a0ae94461fdcca090b348cd5e0c963c666dc3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S0026-0495(03)00191-4$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>315,781,785,3551,27926,27927,45997</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15214898$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14564680$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Rao, Manjunath N</creatorcontrib><creatorcontrib>Marmillot, Philippe</creatorcontrib><creatorcontrib>Gong, Maokaı̈</creatorcontrib><creatorcontrib>Palmer, David A</creatorcontrib><creatorcontrib>Seeff, Leonard B</creatorcontrib><creatorcontrib>Strader, Doris B</creatorcontrib><creatorcontrib>Lakshman, M.Raj</creatorcontrib><title>Light, but not heavy alcohol drinking, stimulates paraoxonase by upregulating liver mRNA in rats and humans</title><title>Metabolism, clinical and experimental</title><addtitle>Metabolism</addtitle><description><![CDATA[Paraoxonase 1 (PON) may contribute to the cardioprotective action of high-density lipoprotein (HDL) because it inhibits low-density lipoprotein (LDL) oxidation, a prerequisite for the onset of atherosclerosis. Because light drinking and heavy drinking have diametrically opposite effects on cardioprotection, we have determined the effects of ethanol dosage on rat serum PON activity and its hepatic expression. Furthermore, we have investigated PON activity and polymorphism in human light and heavy drinkers. Our results confirm that HDL-PON inhibited LDL oxidation, destroyed oxidized LDL, and inhibited its uptake by macrophages. Light ethanol feeding caused a 20% to 25% (
P < .05) increase in PON activity in both serum and liver and a 59% (
P < .001) increase in the level of liver PON mRNA compared with pair-fed control rats. In contrast, heavy ethanol feeding caused a 25% (
P < .05) decrease in serum and liver PON activities with a 51% (
P < .01) decrease in liver PON mRNA level. Light drinkers had a 395% (
P < .001) higher, whereas heavy drinkers had a 45% (
P < .001) lower serum PON activity compared with nondrinkers. Significantly, the number of homozygotes versus heterozygotes with respect to high or low activity PON phenotype was similar in all the groups. Therefore, we conclude that light drinking upregulates, whereas heavy drinking downregulates PON activity and its expression, irrespective of its genetic polymorphism.]]></description><subject>Adult</subject><subject>Alcohol Drinking - blood</subject><subject>Alcohol Drinking - metabolism</subject><subject>Alcoholism and acute alcohol poisoning</subject><subject>Animals</subject><subject>Aryldialkylphosphatase</subject><subject>Biological and medical sciences</subject><subject>Cardiotonic Agents - administration & dosage</subject><subject>Cardiotonic Agents - pharmacology</subject><subject>Down-Regulation - drug effects</subject><subject>Esterases - blood</subject><subject>Esterases - genetics</subject><subject>Esterases - metabolism</subject><subject>Ethanol - administration & dosage</subject><subject>Ethanol - pharmacology</subject><subject>General aspects</subject><subject>Heterozygote</subject><subject>Homozygote</subject><subject>Humans</subject><subject>Lipoproteins, LDL - metabolism</subject><subject>Liver - enzymology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Oxidation-Reduction - drug effects</subject><subject>Polymorphism, Genetic</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>RNA, Messenger - metabolism</subject><subject>Toxicology</subject><issn>0026-0495</issn><issn>1532-8600</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqF0E1v1DAQgGELgei28BNAvoBAamC8dpz4hKqqfEgrkPg4WxNnsmua2Fs7WbH_nmx3RY-cfPAzY-tl7IWAdwKEfv8DYKkLUKZ8A_ItgDCiUI_YQpRyWdQa4DFb_CNn7Dzn3wBQVbV-ys6EKrXSNSzY7cqvN-Mlb6aRhzjyDeFuz7F3cRN73iYfbn1YX_I8-mHqcaTMt5gw_okBM_Fmz6dtovXhana89ztKfPj-9Yr7wBOOmWNo-WYaMORn7EmHfabnp_OC_fp48_P6c7H69unL9dWqcNKIsUCsNHXgELUiSdRo12hZqVYLhYBklNKia51DMNBIVbu2JHBGS6e1bp28YK-Pe7cp3k2URzv47KjvMVCcsq3E0hgFZoblEboUc07U2W3yA6a9FWAPle19ZXtIaEHa-8pWzXMvTw9MzUDtw9Qp6wxenQBmh32XMDifH1y5FKo29ew-HB3NOXaeks3OU3DU-kRutG30__nKX5yXmuk</recordid><startdate>20031001</startdate><enddate>20031001</enddate><creator>Rao, Manjunath N</creator><creator>Marmillot, Philippe</creator><creator>Gong, Maokaı̈</creator><creator>Palmer, David A</creator><creator>Seeff, Leonard B</creator><creator>Strader, Doris B</creator><creator>Lakshman, M.Raj</creator><general>Elsevier Inc</general><general>Elsevier</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20031001</creationdate><title>Light, but not heavy alcohol drinking, stimulates paraoxonase by upregulating liver mRNA in rats and humans</title><author>Rao, Manjunath N ; Marmillot, Philippe ; Gong, Maokaı̈ ; Palmer, David A ; Seeff, Leonard B ; Strader, Doris B ; Lakshman, M.Raj</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c391t-aa76ef0caa64e3eeb6cb6374d614a0ae94461fdcca090b348cd5e0c963c666dc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Adult</topic><topic>Alcohol Drinking - blood</topic><topic>Alcohol Drinking - metabolism</topic><topic>Alcoholism and acute alcohol poisoning</topic><topic>Animals</topic><topic>Aryldialkylphosphatase</topic><topic>Biological and medical sciences</topic><topic>Cardiotonic Agents - administration & dosage</topic><topic>Cardiotonic Agents - pharmacology</topic><topic>Down-Regulation - drug effects</topic><topic>Esterases - blood</topic><topic>Esterases - genetics</topic><topic>Esterases - metabolism</topic><topic>Ethanol - administration & dosage</topic><topic>Ethanol - pharmacology</topic><topic>General aspects</topic><topic>Heterozygote</topic><topic>Homozygote</topic><topic>Humans</topic><topic>Lipoproteins, LDL - metabolism</topic><topic>Liver - enzymology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Oxidation-Reduction - drug effects</topic><topic>Polymorphism, Genetic</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>RNA, Messenger - metabolism</topic><topic>Toxicology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Rao, Manjunath N</creatorcontrib><creatorcontrib>Marmillot, Philippe</creatorcontrib><creatorcontrib>Gong, Maokaı̈</creatorcontrib><creatorcontrib>Palmer, David A</creatorcontrib><creatorcontrib>Seeff, Leonard B</creatorcontrib><creatorcontrib>Strader, Doris B</creatorcontrib><creatorcontrib>Lakshman, M.Raj</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Metabolism, clinical and experimental</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Rao, Manjunath N</au><au>Marmillot, Philippe</au><au>Gong, Maokaı̈</au><au>Palmer, David A</au><au>Seeff, Leonard B</au><au>Strader, Doris B</au><au>Lakshman, M.Raj</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Light, but not heavy alcohol drinking, stimulates paraoxonase by upregulating liver mRNA in rats and humans</atitle><jtitle>Metabolism, clinical and experimental</jtitle><addtitle>Metabolism</addtitle><date>2003-10-01</date><risdate>2003</risdate><volume>52</volume><issue>10</issue><spage>1287</spage><epage>1294</epage><pages>1287-1294</pages><issn>0026-0495</issn><eissn>1532-8600</eissn><abstract><![CDATA[Paraoxonase 1 (PON) may contribute to the cardioprotective action of high-density lipoprotein (HDL) because it inhibits low-density lipoprotein (LDL) oxidation, a prerequisite for the onset of atherosclerosis. Because light drinking and heavy drinking have diametrically opposite effects on cardioprotection, we have determined the effects of ethanol dosage on rat serum PON activity and its hepatic expression. Furthermore, we have investigated PON activity and polymorphism in human light and heavy drinkers. Our results confirm that HDL-PON inhibited LDL oxidation, destroyed oxidized LDL, and inhibited its uptake by macrophages. Light ethanol feeding caused a 20% to 25% (
P < .05) increase in PON activity in both serum and liver and a 59% (
P < .001) increase in the level of liver PON mRNA compared with pair-fed control rats. In contrast, heavy ethanol feeding caused a 25% (
P < .05) decrease in serum and liver PON activities with a 51% (
P < .01) decrease in liver PON mRNA level. Light drinkers had a 395% (
P < .001) higher, whereas heavy drinkers had a 45% (
P < .001) lower serum PON activity compared with nondrinkers. Significantly, the number of homozygotes versus heterozygotes with respect to high or low activity PON phenotype was similar in all the groups. Therefore, we conclude that light drinking upregulates, whereas heavy drinking downregulates PON activity and its expression, irrespective of its genetic polymorphism.]]></abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>14564680</pmid><doi>10.1016/S0026-0495(03)00191-4</doi><tpages>8</tpages></addata></record> |
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| ispartof | Metabolism, clinical and experimental, 2003-10, Vol.52 (10), p.1287-1294 |
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| subjects | Adult Alcohol Drinking - blood Alcohol Drinking - metabolism Alcoholism and acute alcohol poisoning Animals Aryldialkylphosphatase Biological and medical sciences Cardiotonic Agents - administration & dosage Cardiotonic Agents - pharmacology Down-Regulation - drug effects Esterases - blood Esterases - genetics Esterases - metabolism Ethanol - administration & dosage Ethanol - pharmacology General aspects Heterozygote Homozygote Humans Lipoproteins, LDL - metabolism Liver - enzymology Male Medical sciences Middle Aged Oxidation-Reduction - drug effects Polymorphism, Genetic Rats Rats, Wistar RNA, Messenger - metabolism Toxicology |
| title | Light, but not heavy alcohol drinking, stimulates paraoxonase by upregulating liver mRNA in rats and humans |
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