H. Fukushima, S. Aono, Y. Nakamura, M. Endo, T. Imai
{"title":"The effect of N-(α-methylbenzyl)linoleamide on cholesterol metabolism in rats","authors":"H. Fukushima, S. Aono, Y. Nakamura, M. Endo, T. Imai","doi":"10.1016/S0368-1319(69)80043-8","DOIUrl":null,"url":null,"abstract":"<div><p></p><ul><li><span>(1)</span><span><p>The effect of <span>dl</span>-<em>N</em>-(<em>α</em>-methylbenzyl) linoleamide (MBLA) and its optically active isomers (<span>d</span>-MBLA and <span>l</span>-MBLA) on cholesterol metabolism was studied in rats. After administering MBLA, <span>d</span>-MBLA and <span>l</span>-BMLA with [4-<sup>14</sup>C]cholesterol, total [4-<sup>14</sup>C]cholesterol levels in the plasma and liver, and its ester ratio in the liver were markedly depressed after 4 h. After 8 h, the same results were obtained, and the esterified [4-<sup>14</sup>C]cholesterol ratio in the small intestine was also depressed, but there was no significant difference after 24 h. The inhibitory effect on plasma and liver [4-<sup>14</sup>C]cholesterol pools was in the order <span>d</span>-MBLA > MBLA > <span>l</span>-MBLA.</p></span></li><li><span>(2)</span><span><p>The cholesterol-lowering effect of MBLA was not decreased after administering it for 4 weeks.</p></span></li><li><span>(3)</span><span><p>After administering MBLA, <span>d</span>-MBLA and <span>l</span>-MBLA with [<sup>3</sup>H] cholesterol to thoracic-duct fistula rats, total [<sup>3</sup>H]cholesterol levels and its ester ratio in lymph were markedly depressed for 24 h. These results suggest that the cholesterol-lowering mechanism of these compounds is due to reduced cholesterol absorption from the intestines.</p></span></li><li><span>(4)</span><span><p>Hepatic cholesterogenesis was accelerated when a diet containing 0.1 % of MBLA was administered for 1–2 weeks. The acceleration of cholesterol biosynthesis by inhibitors of cholesterol absorption is considered to be due to a homeostatic mechanism that maintains body cholesterol via a feedback control.</p></span></li></ul></div>","PeriodicalId":78351,"journal":{"name":"Journal of atherosclerosis research","volume":"10 3","pages":"Pages 403-414"},"PeriodicalIF":0.0000,"publicationDate":"1969-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0368-1319(69)80043-8","citationCount":"31","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of atherosclerosis research","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0368131969800438","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 31
Abstract
(1)
The effect of dl-N-(α-methylbenzyl) linoleamide (MBLA) and its optically active isomers (d-MBLA and l-MBLA) on cholesterol metabolism was studied in rats. After administering MBLA, d-MBLA and l-BMLA with [4-14C]cholesterol, total [4-14C]cholesterol levels in the plasma and liver, and its ester ratio in the liver were markedly depressed after 4 h. After 8 h, the same results were obtained, and the esterified [4-14C]cholesterol ratio in the small intestine was also depressed, but there was no significant difference after 24 h. The inhibitory effect on plasma and liver [4-14C]cholesterol pools was in the order d-MBLA > MBLA > l-MBLA.
(2)
The cholesterol-lowering effect of MBLA was not decreased after administering it for 4 weeks.
(3)
After administering MBLA, d-MBLA and l-MBLA with [3H] cholesterol to thoracic-duct fistula rats, total [3H]cholesterol levels and its ester ratio in lymph were markedly depressed for 24 h. These results suggest that the cholesterol-lowering mechanism of these compounds is due to reduced cholesterol absorption from the intestines.
(4)
Hepatic cholesterogenesis was accelerated when a diet containing 0.1 % of MBLA was administered for 1–2 weeks. The acceleration of cholesterol biosynthesis by inhibitors of cholesterol absorption is considered to be due to a homeostatic mechanism that maintains body cholesterol via a feedback control.