{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,2]],"date-time":"2025-11-02T10:21:50Z","timestamp":1762078910013,"version":"3.37.0"},"reference-count":50,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"2","license":[{"start":{"date-parts":[[2015,9,1]],"date-time":"2015-09-01T00:00:00Z","timestamp":1441065600000},"content-version":"tdm","delay-in-days":9708,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[1989,2]]},"abstract":"<jats:sec>\n            <jats:title\/>\n            <jats:p>Effects of chronic ethanol consumption on serum lip-oproteins have been studied in the rat. The serum levels of triglycerides, cholesterol, phospholipids and apolipo-proteins AI and AIV increased significantly after 1 week of ethanol feeding, and they remained elevated up to 7 weeks of alcohol drinking. By contrast, serum total apolipoprotein E decreased or, sometimes, did not change. Very-low-density lipoprotein cholesterol, triglycerides and very-low-density lipoprotein apolipoprotein E of the alcohol-fed rats increased in parallel and were about 2-to 2.5-fold over the controls. Whereas high-density lipoprotein cholesterol, phospholipids, apolipoprotein AI and AIV increased 1.2-fold by chronic alcohol feeding, the level of high-density lipoprotein apolipoprotein E decreased to 70% of that of the control rats. The rates of secretion of apolipoprotein AI, E and AIV into the culture medium by hepatocytes isolated from ethanol-fed rats were 1.8-, 1.3-and 1.1-fold higher than those from control rats. These data indicate that (i) chronic ethanol feeding increases very-low-density lipoprotein and high-density lipoprotein in the rat; (ii) serum high-density lipoprotein particles of the ethanol-fed rats are deficient in apolipoprotein E, and (iii) chronic ethanol feeding increases hepatic secretion of apolipoprotein AI, E and AIV. Since the steady-state serum level of apolipoprotein E decreases or remains unchanged in the presence of increased hepatic apolipoprotein E secretion, this imbalance suggests that alcohol feeding either accelerates the rate of degradation of serum apolipoprotein E or suppresses apolipoprotein E synthesis by nonhepatic tissues.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1002\/hep.1840090224","type":"journal-article","created":{"date-parts":[[2007,3,3]],"date-time":"2007-03-03T22:57:43Z","timestamp":1172962663000},"page":"307-313","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":18,"title":["Serum high-density lipoprotein particles of alcohol-fed rats are deficient in apolipoprotein E"],"prefix":"10.1097","volume":"9","author":[{"given":"Renee C.","family":"Lin","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lawrence","family":"Lumeng","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Vickie L.","family":"Phelps","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"276","reference":[{"key":"10.1002\/hep.1840090224-BIB1","doi-asserted-by":"crossref","first-page":"1128","DOI":"10.1001\/archinte.1981.00340090024008","volume":"141","author":"Gordon","year":"1981","journal-title":"Arch Intern Med"},{"key":"10.1002\/hep.1840090224-BIB2","doi-asserted-by":"crossref","first-page":"707","DOI":"10.1016\/0002-9343(77)90874-9","volume":"62","author":"Gordon","year":"1977","journal-title":"Am J Med"},{"key":"10.1002\/hep.1840090224-BIB3","doi-asserted-by":"crossref","first-page":"888","DOI":"10.1093\/oxfordjournals.aje.a113376","volume":"115","author":"Barrett-Conner","year":"1982","journal-title":"Am J Epidemiol"},{"key":"10.1002\/hep.1840090224-BIB4","doi-asserted-by":"crossref","first-page":"48","DOI":"10.1016\/S0022-2275(20)39435-9","volume":"13","author":"Lefevre","year":"1972","journal-title":"J Lipid Res"},{"key":"10.1002\/hep.1840090224-BIB5","first-page":"563","volume":"26","author":"Hirayama","year":"1979","journal-title":"Res Commun Chem Pathol Pharmacol"},{"key":"10.1002\/hep.1840090224-BIB6","doi-asserted-by":"crossref","first-page":"245","DOI":"10.1093\/ajcn\/36.2.245","volume":"26","author":"Topping","year":"1982","journal-title":"Am J Clin Nutr"},{"key":"10.1002\/hep.1840090224-BIB7","doi-asserted-by":"crossref","first-page":"144","DOI":"10.1161\/01.ATV.1.2.144","volume":"1","author":"Rudel","year":"1981","journal-title":"Arteriosclerosis"},{"key":"10.1002\/hep.1840090224-BIB8","first-page":"384","volume":"77","author":"Kudzma","year":"1971","journal-title":"J Lab Clin Med"},{"key":"10.1002\/hep.1840090224-BIB9","doi-asserted-by":"crossref","first-page":"296","DOI":"10.1172\/JCI107185","volume":"52","author":"Baraona","year":"1973","journal-title":"J Clin Invest"},{"key":"10.1002\/hep.1840090224-BIB10","doi-asserted-by":"crossref","first-page":"112","DOI":"10.1016\/0026-0495(85)90118-0","volume":"34","author":"Taskinen","year":"1985","journal-title":"Metabolism"},{"key":"10.1002\/hep.1840090224-BIB11","doi-asserted-by":"crossref","first-page":"275","DOI":"10.1016\/0021-9150(83)90178-8","volume":"46","author":"Fraser","year":"1983","journal-title":"Atherosclerosis"},{"key":"10.1002\/hep.1840090224-BIB12","first-page":"524","volume":"34","author":"Williams","year":"1985","journal-title":"Me tabolism"},{"key":"10.1002\/hep.1840090224-BIB13","first-page":"181","volume-title":"Disturbances in lipid and lipoprotein metabolism","author":"Mahley","year":"1978","unstructured":"Alterations in plasma lipoproteins induced by cholesterol feeding in animals including man. 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