YM‐53601, a novel squalene synthase inhibitor, suppresses lipogenic biosynthesis and lipid secretion in rodents
To better understand how it decreases plasma cholesterol and triglyceride levels, we evaluated the effect of (E)‐2‐[2‐fluoro‐2‐(quinuclidin‐3‐ylidene)ethoxy]‐9H‐carbazole monohydrochloride(YM‐53601) on lipogenic biosynthesis in the liver and lipid secretion from the liver in rats and hamsters. Singl...
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| creator | Ugawa, Tohru Kakuta, Hirotoshi Moritani, Hiroshi Inagaki, Osamu Shikama, Hisataka |
| description | To better understand how it decreases plasma cholesterol and triglyceride levels, we evaluated the effect of (E)‐2‐[2‐fluoro‐2‐(quinuclidin‐3‐ylidene)ethoxy]‐9H‐carbazole monohydrochloride(YM‐53601) on lipogenic biosynthesis in the liver and lipid secretion from the liver in rats and hamsters.
Single administration of YM‐53601 in cholestyramine‐treated rats inhibited triglyceride and free fatty acid (FFA) biosynthesis at a similar dose range to that at which it inhibited cholesterol biosynthesis. YM‐53601 inhibited both triglyceride and FFA biosynthesis in hamsters treated with cholestyramine.
YM‐53601 by single oral administration decreased the enhanced plasma triglyceride levels in hamsters induced by an injection of protamine sulfate, which inhibits lipoprotein lipase (LPL) and consequently increases plasma very low‐density lipoprotein (VLDL) triglyceride levels. YM‐53601 also decreased the enhanced plasma triglyceride and cholesterol levels in hamsters treated with Triton WR1339, which also inhibits the degradation of VLDL. Plasma cholesterol was significantly decreased as soon as 1 h after single administration of YM‐53601 in hamsters fed a normal diet.
This is the first report that a squalene synthase inhibitor suppresses lipogenic biosynthesis in the liver and cholesterol and triglyceride secretion from the liver in vivo. We therefore suggest that the mechanism by which YM‐53601 decreases plasma triglyceride might include these effects. The finding that YM‐53601 rapidly decreased plasma cholesterol suggests that this compound may be effective in decreasing plasma cholesterol levels early in the course of treatment of hypercholesterolemia in humans.
British Journal of Pharmacology (2003) 139, 140–146. doi:10.1038/sj.bjp.0705229 |
| doi_str_mv | 10.1038/sj.bjp.0705229 |
| format | Article |
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Single administration of YM‐53601 in cholestyramine‐treated rats inhibited triglyceride and free fatty acid (FFA) biosynthesis at a similar dose range to that at which it inhibited cholesterol biosynthesis. YM‐53601 inhibited both triglyceride and FFA biosynthesis in hamsters treated with cholestyramine.
YM‐53601 by single oral administration decreased the enhanced plasma triglyceride levels in hamsters induced by an injection of protamine sulfate, which inhibits lipoprotein lipase (LPL) and consequently increases plasma very low‐density lipoprotein (VLDL) triglyceride levels. YM‐53601 also decreased the enhanced plasma triglyceride and cholesterol levels in hamsters treated with Triton WR1339, which also inhibits the degradation of VLDL. Plasma cholesterol was significantly decreased as soon as 1 h after single administration of YM‐53601 in hamsters fed a normal diet.
This is the first report that a squalene synthase inhibitor suppresses lipogenic biosynthesis in the liver and cholesterol and triglyceride secretion from the liver in vivo. We therefore suggest that the mechanism by which YM‐53601 decreases plasma triglyceride might include these effects. The finding that YM‐53601 rapidly decreased plasma cholesterol suggests that this compound may be effective in decreasing plasma cholesterol levels early in the course of treatment of hypercholesterolemia in humans.
British Journal of Pharmacology (2003) 139, 140–146. doi:10.1038/sj.bjp.0705229</description><identifier>ISSN: 0007-1188</identifier><identifier>EISSN: 1476-5381</identifier><identifier>DOI: 10.1038/sj.bjp.0705229</identifier><identifier>PMID: 12746232</identifier><identifier>CODEN: BJPCBM</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Animals ; Anticholesteremic Agents - pharmacology ; Biological and medical sciences ; biosynthesis ; cholesterol ; Cholesterol - biosynthesis ; Cholesterol - blood ; Cholesterol - secretion ; Cholestyramine Resin - pharmacology ; Cricetinae ; Farnesyl-Diphosphate Farnesyltransferase - antagonists & inhibitors ; Fatty Acids, Nonesterified - biosynthesis ; Fatty Acids, Nonesterified - blood ; Fatty Acids, Nonesterified - metabolism ; lipogenesis ; Lipoprotein Lipase - antagonists & inhibitors ; Liver - drug effects ; Liver - metabolism ; Liver - secretion ; Male ; Medical sciences ; Mesocricetus ; Polyethylene Glycols - pharmacology ; protamine sulfate ; Protamines - pharmacology ; Quinuclidines - pharmacology ; Rats ; Rats, Sprague-Dawley ; secretion ; squalene synthase ; triglyceride ; Triglycerides - biosynthesis ; Triglycerides - blood ; Triglycerides - secretion ; Triton WR1339 ; YM‐53601</subject><ispartof>British journal of pharmacology, 2003-05, Vol.139 (1), p.140-146</ispartof><rights>2003 British Pharmacological Society</rights><rights>2003 INIST-CNRS</rights><rights>Copyright Nature Publishing Group May 2003</rights><rights>Copyright 2003, Nature Publishing Group 2003 Nature Publishing Group</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4878-9ba6a5a91fe214f07cd97d28827057adf24ea3acd747e091dedf44883c322d2d3</citedby><cites>FETCH-LOGICAL-c4878-9ba6a5a91fe214f07cd97d28827057adf24ea3acd747e091dedf44883c322d2d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1573827/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1573827/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,1417,1433,27924,27925,45574,45575,46409,46833,53791,53793</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14764979$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12746232$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ugawa, Tohru</creatorcontrib><creatorcontrib>Kakuta, Hirotoshi</creatorcontrib><creatorcontrib>Moritani, Hiroshi</creatorcontrib><creatorcontrib>Inagaki, Osamu</creatorcontrib><creatorcontrib>Shikama, Hisataka</creatorcontrib><title>YM‐53601, a novel squalene synthase inhibitor, suppresses lipogenic biosynthesis and lipid secretion in rodents</title><title>British journal of pharmacology</title><addtitle>Br J Pharmacol</addtitle><description>To better understand how it decreases plasma cholesterol and triglyceride levels, we evaluated the effect of (E)‐2‐[2‐fluoro‐2‐(quinuclidin‐3‐ylidene)ethoxy]‐9H‐carbazole monohydrochloride(YM‐53601) on lipogenic biosynthesis in the liver and lipid secretion from the liver in rats and hamsters.
Single administration of YM‐53601 in cholestyramine‐treated rats inhibited triglyceride and free fatty acid (FFA) biosynthesis at a similar dose range to that at which it inhibited cholesterol biosynthesis. YM‐53601 inhibited both triglyceride and FFA biosynthesis in hamsters treated with cholestyramine.
YM‐53601 by single oral administration decreased the enhanced plasma triglyceride levels in hamsters induced by an injection of protamine sulfate, which inhibits lipoprotein lipase (LPL) and consequently increases plasma very low‐density lipoprotein (VLDL) triglyceride levels. YM‐53601 also decreased the enhanced plasma triglyceride and cholesterol levels in hamsters treated with Triton WR1339, which also inhibits the degradation of VLDL. Plasma cholesterol was significantly decreased as soon as 1 h after single administration of YM‐53601 in hamsters fed a normal diet.
This is the first report that a squalene synthase inhibitor suppresses lipogenic biosynthesis in the liver and cholesterol and triglyceride secretion from the liver in vivo. We therefore suggest that the mechanism by which YM‐53601 decreases plasma triglyceride might include these effects. The finding that YM‐53601 rapidly decreased plasma cholesterol suggests that this compound may be effective in decreasing plasma cholesterol levels early in the course of treatment of hypercholesterolemia in humans.
British Journal of Pharmacology (2003) 139, 140–146. doi:10.1038/sj.bjp.0705229</description><subject>Animals</subject><subject>Anticholesteremic Agents - pharmacology</subject><subject>Biological and medical sciences</subject><subject>biosynthesis</subject><subject>cholesterol</subject><subject>Cholesterol - biosynthesis</subject><subject>Cholesterol - blood</subject><subject>Cholesterol - secretion</subject><subject>Cholestyramine Resin - pharmacology</subject><subject>Cricetinae</subject><subject>Farnesyl-Diphosphate Farnesyltransferase - antagonists & inhibitors</subject><subject>Fatty Acids, Nonesterified - biosynthesis</subject><subject>Fatty Acids, Nonesterified - blood</subject><subject>Fatty Acids, Nonesterified - metabolism</subject><subject>lipogenesis</subject><subject>Lipoprotein Lipase - antagonists & inhibitors</subject><subject>Liver - drug effects</subject><subject>Liver - metabolism</subject><subject>Liver - secretion</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mesocricetus</subject><subject>Polyethylene Glycols - pharmacology</subject><subject>protamine sulfate</subject><subject>Protamines - pharmacology</subject><subject>Quinuclidines - pharmacology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>secretion</subject><subject>squalene synthase</subject><subject>triglyceride</subject><subject>Triglycerides - biosynthesis</subject><subject>Triglycerides - blood</subject><subject>Triglycerides - secretion</subject><subject>Triton WR1339</subject><subject>YM‐53601</subject><issn>0007-1188</issn><issn>1476-5381</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqFkr2O1DAUhSMEYoeFlhJZSFBtBv8kcdKsBCtgkRZBAQWV5dg3O44ydsY3WTQdj8Az8iR4mIgFGioX57vn_hxn2WNG14yK-gX267Yf11TSkvPmTrZihazyUtTsbrailMqcsbo-yR4g9pQmUZb3sxPGZVFxwVfZ7sv7H9--l6Ki7Ixo4sMNDAR3sx7AA8G9nzYagTi_ca2bQjwjOI9jBERAMrgxXIN3hrQu_GIBHRLt7UFyliCYCJMLPhmQGCz4CR9m9zo9IDxa3tPs85vXny4u86sPb99dvLzKTVHLOm9aXelSN6wDzoqOSmMbaXld87Sq1LbjBWihjZWFBNowC7YriroWRnBuuRWn2fnRd5zbLViTekc9qDG6rY57FbRTfyvebdR1uFGslCJ1SQbPF4MYdjPgpLYODQyD9hBmVFLwipfyAD79B-zDHH1aTnEm0_klZQlaHyETA2KE7vckjKpDlAp7laJUS5Sp4Mmf89_iS3YJeLYAGo0euqi9cXjLpY9QNPJgJI7cVzfA_j9t1auPl0WTzvgTE9m7BQ</recordid><startdate>200305</startdate><enddate>200305</enddate><creator>Ugawa, Tohru</creator><creator>Kakuta, Hirotoshi</creator><creator>Moritani, Hiroshi</creator><creator>Inagaki, Osamu</creator><creator>Shikama, Hisataka</creator><general>Blackwell Publishing Ltd</general><general>Nature Publishing</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>3V.</scope><scope>7QP</scope><scope>7RV</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>200305</creationdate><title>YM‐53601, a novel squalene synthase inhibitor, suppresses lipogenic biosynthesis and lipid secretion in rodents</title><author>Ugawa, Tohru ; Kakuta, Hirotoshi ; Moritani, Hiroshi ; Inagaki, Osamu ; Shikama, Hisataka</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4878-9ba6a5a91fe214f07cd97d28827057adf24ea3acd747e091dedf44883c322d2d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Animals</topic><topic>Anticholesteremic Agents - pharmacology</topic><topic>Biological and medical sciences</topic><topic>biosynthesis</topic><topic>cholesterol</topic><topic>Cholesterol - biosynthesis</topic><topic>Cholesterol - blood</topic><topic>Cholesterol - secretion</topic><topic>Cholestyramine Resin - pharmacology</topic><topic>Cricetinae</topic><topic>Farnesyl-Diphosphate Farnesyltransferase - antagonists & inhibitors</topic><topic>Fatty Acids, Nonesterified - biosynthesis</topic><topic>Fatty Acids, Nonesterified - blood</topic><topic>Fatty Acids, Nonesterified - metabolism</topic><topic>lipogenesis</topic><topic>Lipoprotein Lipase - antagonists & inhibitors</topic><topic>Liver - drug effects</topic><topic>Liver - metabolism</topic><topic>Liver - secretion</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mesocricetus</topic><topic>Polyethylene Glycols - pharmacology</topic><topic>protamine sulfate</topic><topic>Protamines - pharmacology</topic><topic>Quinuclidines - pharmacology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>secretion</topic><topic>squalene synthase</topic><topic>triglyceride</topic><topic>Triglycerides - biosynthesis</topic><topic>Triglycerides - blood</topic><topic>Triglycerides - secretion</topic><topic>Triton WR1339</topic><topic>YM‐53601</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ugawa, Tohru</creatorcontrib><creatorcontrib>Kakuta, Hirotoshi</creatorcontrib><creatorcontrib>Moritani, Hiroshi</creatorcontrib><creatorcontrib>Inagaki, Osamu</creatorcontrib><creatorcontrib>Shikama, Hisataka</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>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Proquest Nursing & Allied Health Source</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>British journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ugawa, Tohru</au><au>Kakuta, Hirotoshi</au><au>Moritani, Hiroshi</au><au>Inagaki, Osamu</au><au>Shikama, Hisataka</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>YM‐53601, a novel squalene synthase inhibitor, suppresses lipogenic biosynthesis and lipid secretion in rodents</atitle><jtitle>British journal of pharmacology</jtitle><addtitle>Br J Pharmacol</addtitle><date>2003-05</date><risdate>2003</risdate><volume>139</volume><issue>1</issue><spage>140</spage><epage>146</epage><pages>140-146</pages><issn>0007-1188</issn><eissn>1476-5381</eissn><coden>BJPCBM</coden><abstract>To better understand how it decreases plasma cholesterol and triglyceride levels, we evaluated the effect of (E)‐2‐[2‐fluoro‐2‐(quinuclidin‐3‐ylidene)ethoxy]‐9H‐carbazole monohydrochloride(YM‐53601) on lipogenic biosynthesis in the liver and lipid secretion from the liver in rats and hamsters.
Single administration of YM‐53601 in cholestyramine‐treated rats inhibited triglyceride and free fatty acid (FFA) biosynthesis at a similar dose range to that at which it inhibited cholesterol biosynthesis. YM‐53601 inhibited both triglyceride and FFA biosynthesis in hamsters treated with cholestyramine.
YM‐53601 by single oral administration decreased the enhanced plasma triglyceride levels in hamsters induced by an injection of protamine sulfate, which inhibits lipoprotein lipase (LPL) and consequently increases plasma very low‐density lipoprotein (VLDL) triglyceride levels. YM‐53601 also decreased the enhanced plasma triglyceride and cholesterol levels in hamsters treated with Triton WR1339, which also inhibits the degradation of VLDL. Plasma cholesterol was significantly decreased as soon as 1 h after single administration of YM‐53601 in hamsters fed a normal diet.
This is the first report that a squalene synthase inhibitor suppresses lipogenic biosynthesis in the liver and cholesterol and triglyceride secretion from the liver in vivo. We therefore suggest that the mechanism by which YM‐53601 decreases plasma triglyceride might include these effects. The finding that YM‐53601 rapidly decreased plasma cholesterol suggests that this compound may be effective in decreasing plasma cholesterol levels early in the course of treatment of hypercholesterolemia in humans.
British Journal of Pharmacology (2003) 139, 140–146. doi:10.1038/sj.bjp.0705229</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>12746232</pmid><doi>10.1038/sj.bjp.0705229</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Anticholesteremic Agents - pharmacology Biological and medical sciences biosynthesis cholesterol Cholesterol - biosynthesis Cholesterol - blood Cholesterol - secretion Cholestyramine Resin - pharmacology Cricetinae Farnesyl-Diphosphate Farnesyltransferase - antagonists & inhibitors Fatty Acids, Nonesterified - biosynthesis Fatty Acids, Nonesterified - blood Fatty Acids, Nonesterified - metabolism lipogenesis Lipoprotein Lipase - antagonists & inhibitors Liver - drug effects Liver - metabolism Liver - secretion Male Medical sciences Mesocricetus Polyethylene Glycols - pharmacology protamine sulfate Protamines - pharmacology Quinuclidines - pharmacology Rats Rats, Sprague-Dawley secretion squalene synthase triglyceride Triglycerides - biosynthesis Triglycerides - blood Triglycerides - secretion Triton WR1339 YM‐53601 |
| title | YM‐53601, a novel squalene synthase inhibitor, suppresses lipogenic biosynthesis and lipid secretion in rodents |
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