Implitapide, a Microsomal Triglyceride Transfer Protein Inhibitor, Reduces Progression of Atherosclerosis in Apolipoprotein E Knockout Mice Fed a Western-Type Diet: Involvement of the Inhibition of Postprandial Triglyceride Elevation
Microsomal triglyceride transfer protein (MTP) is essential for the synthesis of both chylomicron in the intestine and very low-density lipoprotein in the liver. An MTP inhibitor, (2S)-2-cyclopentyl-2-[4-[(2,4-dimethyl-9H-pyrido[2,3-b]indol-9-yl)methyl]phenyl]-N-[(1S)-2-hydroxy-1-phenylethyl]ethanam...
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| Published in | Biological & Pharmaceutical Bulletin Vol. 28; no. 2; pp. 247 - 252 |
|---|---|
| Main Authors | , , , , , |
| Format | Journal Article |
| Language | English |
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Japan
The Pharmaceutical Society of Japan
01.02.2005
Pharmaceutical Society of Japan |
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| Abstract | Microsomal triglyceride transfer protein (MTP) is essential for the synthesis of both chylomicron in the intestine and very low-density lipoprotein in the liver. An MTP inhibitor, (2S)-2-cyclopentyl-2-[4-[(2,4-dimethyl-9H-pyrido[2,3-b]indol-9-yl)methyl]phenyl]-N-[(1S)-2-hydroxy-1-phenylethyl]ethanamide (implitapide), has been shown to suppress atherosclerosis in apolipoprotein E knockout (apoE KO) mice. To elucidate the antiatherosclerotic mechanisms of implitapide in the mice, we examined the effects on plasma lipid levels, triglyceride (TG) elevation after oral fat loading, and development of atherosclerosis in apoE KO mice fed a Western-type diet. Implitapide at a dosage of approximately 3.2 mg/kg/day significantly reduced both total cholesterol and TG levels during the 8-week treatment period. In addition, implitapide significantly inhibited the increase in plasma TG levels after oral olive oil loading tests conducted after 4 weeks of treatment. After the treatment, implitapide significantly suppressed the atherosclerotic lesion area by 83% compared with a control group. These results provide direct evidence that the antiatherosclerotic effects of implitapide in apoE KO mice are associated with the inhibition of postprandial TG elevation, in addition to the reduction of both plasma total cholesterol and TG levels. |
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| AbstractList | Microsomal triglyceride transfer protein (MTP) is essential for the synthesis of both chylomicron in the intestine and very low-density lipoprotein in the liver. An MTP inhibitor, (2S)-2-cyclopentyl-2-[4-[(2,4-dimethyl-9H-pyrido[2,3-b]indol-9-yl)methyl]phenyl]-N-[(1S)-2-hydroxy-1-phenylethyl]ethanamide (implitapide), has been shown to suppress atherosclerosis in apolipoprotein E knockout (apoE KO) mice. To elucidate the antiatherosclerotic mechanisms of implitapide in the mice, we examined the effects on plasma lipid levels, triglyceride (TG) elevation after oral fat loading, and development of atherosclerosis in apoE KO mice fed a Western-type diet. Implitapide at a dosage of approximately 3.2 mg/kg/day significantly reduced both total cholesterol and TG levels during the 8-week treatment period. In addition, implitapide significantly inhibited the increase in plasma TG levels after oral olive oil loading tests conducted after 4 weeks of treatment. After the treatment, implitapide significantly suppressed the atherosclerotic lesion area by 83% compared with a control group. These results provide direct evidence that the antiatherosclerotic effects of implitapide in apoE KO mice are associated with the inhibition of postprandial TG elevation, in addition to the reduction of both plasma total cholesterol and TG levels. Microsomal triglyceride transfer protein (MTP) is essential for the synthesis of both chylomicron in the intestine and very low-density lipoprotein in the liver. An MTP inhibitor, (25)-2-cyclopentyl-2-[4-[(2, 4-dimethyl9H-pyrido [2, 3-b]indol-9-yl)methyl] phenyl] -N- [(1S)-2-hydroxy- 1-phenylethyl] ethanamide (implitapide), has been shown to suppress atherosclerosis in apolipoprotein E knockout (apoE KO) mice. To elucidate the antiatherosclerotic mechanisms of implitapide in the mice, we examined the effects on plasma lipid levels, triglyceride (TG) elevation after oral fat loading, and development of atherosclerosis in apoE KO mice fed a Western-type diet. Implitapide at a dosage of approximately 3.2 mg/kg/day significantly reduced both total cholesterol and TG levels during the 8-week treatment period. In addition, implitapide significantly inhibited the increase in plasma TG levels after oral olive oil loading tests conducted after 4 weeks of treatment. After the treatment, implitapide significantly suppressed the atherosclerotic lesion area by 83% compared with a control group. These results provide direct evidence that the antiatherosclerotic effects of implitapide in apoE KO mice are associated with the inhibition of postprandial TG elevation, in addition to the reduction of both plasma total cholesterol and TG levels. Microsomal triglyceride transfer protein (MTP) is essential for the synthesis of both chylomicron in the intestine and very low-density lipoprotein in the liver. An MTP inhibitor, (2S)-2-cyclopentyl-2-[4-[(2,4-dimethyl-9H-pyrido[2,3-b]indol-9-yl)methyl]phenyl]-N-[(1S)-2-hydroxy-1-phenylethyl]ethanamide (implitapide), has been shown to suppress atherosclerosis in apolipoprotein E knockout (apoE KO) mice. To elucidate the antiatherosclerotic mechanisms of implitapide in the mice, we examined the effects on plasma lipid levels, triglyceride (TG) elevation after oral fat loading, and development of atherosclerosis in apoE KO mice fed a Western-type diet. Implitapide at a dosage of approximately 3.2 mg/kg/day significantly reduced both total cholesterol and TG levels during the 8-week treatment period. In addition, implitapide significantly inhibited the increase in plasma TG levels after oral olive oil loading tests conducted after 4 weeks of treatment. After the treatment, implitapide significantly suppressed the atherosclerotic lesion area by 83% compared with a control group. These results provide direct evidence that the antiatherosclerotic effects of implitapide in apoE KO mice are associated with the inhibition of postprandial TG elevation, in addition to the reduction of both plasma total cholesterol and TG levels.Microsomal triglyceride transfer protein (MTP) is essential for the synthesis of both chylomicron in the intestine and very low-density lipoprotein in the liver. An MTP inhibitor, (2S)-2-cyclopentyl-2-[4-[(2,4-dimethyl-9H-pyrido[2,3-b]indol-9-yl)methyl]phenyl]-N-[(1S)-2-hydroxy-1-phenylethyl]ethanamide (implitapide), has been shown to suppress atherosclerosis in apolipoprotein E knockout (apoE KO) mice. To elucidate the antiatherosclerotic mechanisms of implitapide in the mice, we examined the effects on plasma lipid levels, triglyceride (TG) elevation after oral fat loading, and development of atherosclerosis in apoE KO mice fed a Western-type diet. Implitapide at a dosage of approximately 3.2 mg/kg/day significantly reduced both total cholesterol and TG levels during the 8-week treatment period. In addition, implitapide significantly inhibited the increase in plasma TG levels after oral olive oil loading tests conducted after 4 weeks of treatment. After the treatment, implitapide significantly suppressed the atherosclerotic lesion area by 83% compared with a control group. These results provide direct evidence that the antiatherosclerotic effects of implitapide in apoE KO mice are associated with the inhibition of postprandial TG elevation, in addition to the reduction of both plasma total cholesterol and TG levels. |
| Author | Akihisa-Umeno, Hitomi Nagayoshi, Akira Matsuo, Masahiko Mutoh, Seitaro Ueshima, Koji Takakura, Shoji |
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| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/15684478$$D View this record in MEDLINE/PubMed |
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| Cites_doi | 10.1016/S0014-2999(01)01419-4 10.1038/365065a0 10.1016/S0002-9149(00)01127-9 10.2741/A614 10.1016/S0008-6363(01)00227-9 10.1021/jm010294e 10.1016/S0009-8981(98)00073-4 10.1194/jlr.M300094-JLR200 10.1067/mhj.2002.130301 10.1016/0092-8674(92)90362-G 10.1016/S0021-9258(18)57092-7 10.1358/dof.2000.025.11.599755 10.1038/362801a0 10.1126/science.1439810 10.1001/jama.285.19.2486 10.1126/science.282.5389.751 10.1172/JCI117460 |
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| References_xml | – reference: 6) Wetterau J. R., Aggerbeck L. P., Bouma M. E., Eisenberg C., Munck A., Hermier M., Schmitz J., Gay G., Rader D. J., Gregg R. E., Science, 258, 999—1001 (1992). – reference: 7) Sharp D., Blinderman L., Combs K. A., Kienzle B., Ricci B., Wager-Smith K., Gil C. M., Turck C. W., Bouma M. E., Rader D. J., Aggerbeck L. P., Gregg R. E., Gordon D. A., Wetterau J. R., Nature (London), 365, 65—69 (1993). – reference: 4) Yu K. C., Cooper A. D., Front. Biosci., 6, D332—D354 (2001). – reference: 8) Chandler C. E., Wilder D. E., Pettini J. L., Savoy Y. E., Petras S. F., Chang G., Vincent J., Harwood H. J., Jr., J. Lipid Res., 44, 1887—1901 (2003). – reference: 13) Tanaka A., Tomie N., Nakano T., Nakajima K., Yui K., Tamura M., Numano F., Clin. Chim. Acta, 275, 43—52 (1998). – reference: 11) Zhang S. H., Reddick R. L., Burkey B., Maeda N., J. Clin. Invest., 94, 937—945 (1994). – reference: 17) Ross R., Nature (London), 362, 801—809 (1993). – reference: 1) Gotto A. M., Jr., Am. Heart J., 144 (Suppl.), S33—S42 (2002). – reference: 5) Wilmink H. W., Twickler M. B., Banga J. D., Dallinga-Thie G. M., Eeltink H., Erkelens D. W., Rabelink T. J., Stroes E. S., Cardiovasc. Res., 50, 577—582 (2001). – reference: 9) Ksander G. M., deJesus R., Yuan A., Fink C., Moskal M., Carlson E., Kukkola P., Bilci N., Wallace E., Neubert A., Feldman D., Mogelesky T., Poirier K., Jeune M., Steele R., Wasvery J., Stephan Z., Cahill E., Webb R., Navarrete A., Lee W., Gibson J., Alexander N., Sharif H., Hospattankar A., J. Med. Chem., 44, 4677—4687 (2001). – reference: 14) van de Kamer J. H., ten Bokkel H. H., Weyers H. A., J. Biol. Chem., 177, 347—355 (1949). – reference: 16) Shiomi M., Ito T., Eur. J. Pharmacol., 431, 127—131 (2001). – reference: 12) Sorbera L. A., Martin L., Silvestre J., Castaner J., Drugs Fut., 25, 1138—1144 (2000). – reference: 3) Cullen P., Am. J. Cardiol., 86, 943—949 (2000). – reference: 10) Plump A. S., Smith J. D., Hayek T., Aalto-Setälä, Walsh A., Verstuyft J. G., Rubin E. M., Breslow J. L., Cell, 71, 343—353 (1992). – reference: 2) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults, JAMA, 285, 2486—2497 (2001). – reference: 15) Wetterau J. R., Gregg R. E., Harrity T. W., Arbeeny C., Cap M., Connolly F., Chu C. H., George R. J., Gordon D. A., Jamil H., Jolibois K. G., Kunselman L. K., Lan S. J., Maccagnan T. J., Ricci B., Yan M., Young D., Chen Y., Fryszman O. M., Logan J. V., Musial C. L., Poss M. A., Robl J. A., Simpkins L. M., Slusarchyk W. A., Sulsky R., Taunk P., Magnin D. R., Tino J. A., Lawrence M., Dickson J. K., Biller S. A., Science, 282, 751—754 (1998). – ident: 16 doi: 10.1016/S0014-2999(01)01419-4 – ident: 7 doi: 10.1038/365065a0 – ident: 3 doi: 10.1016/S0002-9149(00)01127-9 – volume: 6 start-page: D332 issn: 1093-9946 year: 2001 ident: 4 publication-title: Front. Biosci. doi: 10.2741/A614 – ident: 5 doi: 10.1016/S0008-6363(01)00227-9 – ident: 9 doi: 10.1021/jm010294e – ident: 13 doi: 10.1016/S0009-8981(98)00073-4 – ident: 8 doi: 10.1194/jlr.M300094-JLR200 – ident: 1 doi: 10.1067/mhj.2002.130301 – ident: 10 doi: 10.1016/0092-8674(92)90362-G – volume: 177 start-page: 347 issn: 0021-9258 year: 1949 ident: 14 publication-title: J. Biol. Chem. doi: 10.1016/S0021-9258(18)57092-7 – volume: 25 start-page: 1138 issn: 0377-8282 year: 2000 ident: 12 publication-title: Drugs Fut. doi: 10.1358/dof.2000.025.11.599755 – volume: 362 start-page: 801 issn: 0028-0836 year: 1993 ident: 17 publication-title: Nature doi: 10.1038/362801a0 – volume: 258 start-page: 999 issn: 0036-8075 issue: 5084 year: 1992 ident: 6 publication-title: Science doi: 10.1126/science.1439810 – ident: 2 doi: 10.1001/jama.285.19.2486 – ident: 15 doi: 10.1126/science.282.5389.751 – volume: 94 start-page: 937 issn: 0021-9738 year: 1994 ident: 11 publication-title: J. Clin. Invest. doi: 10.1172/JCI117460 |
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| SubjectTerms | Animals Aorta, Thoracic - drug effects Aorta, Thoracic - metabolism Apolipoproteins E - deficiency Apolipoproteins E - genetics Arteriosclerosis - blood Arteriosclerosis - prevention & control atherosclerosis Carrier Proteins - antagonists & inhibitors Carrier Proteins - blood Diet, Atherogenic Dietary Fats - administration & dosage implitapide Indoles - pharmacology Indoles - therapeutic use Male Mice Mice, Inbred C57BL Mice, Knockout microsomal triglyceride transfer protein Postprandial Period - drug effects Postprandial Period - physiology Pyridines - pharmacology Pyridines - therapeutic use Triglycerides - antagonists & inhibitors Triglycerides - blood |
| Title | Implitapide, a Microsomal Triglyceride Transfer Protein Inhibitor, Reduces Progression of Atherosclerosis in Apolipoprotein E Knockout Mice Fed a Western-Type Diet: Involvement of the Inhibition of Postprandial Triglyceride Elevation |
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