The anti-obesity effect of rimonabant is associated with an improved serum lipid profile
We investigated the effects of chronic treatment with the CB1 receptor antagonist rimonabant (10 mg/kg/day p.o. for 10 weeks) in mice with established obesity (5‐month high‐fat diet). Untreated obese mice showed a weight gain of 46% (45.0 ± 0.6 g vs. 30.8 ± 0.5 g) compared with age‐matched animals f...
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description | We investigated the effects of chronic treatment with the CB1 receptor antagonist rimonabant (10 mg/kg/day p.o. for 10 weeks) in mice with established obesity (5‐month high‐fat diet). Untreated obese mice showed a weight gain of 46% (45.0 ± 0.6 g vs. 30.8 ± 0.5 g) compared with age‐matched animals fed a standard diet. Rimonabant treatment, commencing after 5‐month high‐fat diet, produced a marked and sustained decrease in body weight (34.5 ± 0.8 g vs. 47.2 ± 0.5 g in the high‐fat vehicle group, p |
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E. ; Janiak, P. ; Herbert, J.-M.</creator><creatorcontrib>Poirier, B. ; Bidouard, J.-P. ; Cadrouvele, C. ; Marniquet, X. ; Staels, B. ; O'Connor, S. E. ; Janiak, P. ; Herbert, J.-M.</creatorcontrib><description>We investigated the effects of chronic treatment with the CB1 receptor antagonist rimonabant (10 mg/kg/day p.o. for 10 weeks) in mice with established obesity (5‐month high‐fat diet). Untreated obese mice showed a weight gain of 46% (45.0 ± 0.6 g vs. 30.8 ± 0.5 g) compared with age‐matched animals fed a standard diet. Rimonabant treatment, commencing after 5‐month high‐fat diet, produced a marked and sustained decrease in body weight (34.5 ± 0.8 g vs. 47.2 ± 0.5 g in the high‐fat vehicle group, p < 0.001). The anti‐obesity effect of rimonabant was similar to that obtained by switching obese mice from high‐fat diet to standard laboratory diet during 10 weeks (final weight 33.7 ± 0.6 g) and was associated with only transient (14 days) reduction in energy intake. Serum leptin, insulin and glucose levels were markedly elevated in obese animals. Rimonabant treatment significantly reduced these elevations (leptin −81%, insulin −78%, glucose −67%, p < 0.001 in all cases vs. high‐fat vehicle group). In addition, rimonabant treatment modestly but significantly increased serum adiponectin levels (+18%, p < 0.05 vs. high‐fat vehicle group). Obese mice demonstrated abnormal serum lipid profiles. Although rimonabant did not modify high‐density lipoprotein cholesterol (HDLc) and had modest effects on total cholesterol, it significantly reduced triglycerides and low‐density lipoprotein cholesterol (LDLc) and, notably, increased the HDLc/LDLc ratio (12.4 ± 0.8 vs. 7.9 ± 0.2 in high‐fat vehicle group, p < 0.001). Therefore, in a model of established obesity, chronic rimonabant treatment produces a marked and sustained decrease in body weight (equivalent to that achieved by dietary change) which is associated with favourable modifications in serum biochemical and lipid profiles.</description><identifier>ISSN: 1462-8902</identifier><identifier>EISSN: 1463-1326</identifier><identifier>DOI: 10.1111/j.1463-1326.2004.00374.x</identifier><identifier>PMID: 15642077</identifier><language>eng</language><publisher>Oxford, UK; Malden, USA: Blackwell Science Ltd</publisher><subject>Adiponectin ; Animals ; Anti-Obesity Agents - therapeutic use ; Blood Glucose - analysis ; body weight ; CB1 receptor antagonist ; Cholesterol - blood ; Cholesterol, HDL - blood ; food intake ; glucose ; insulin ; Insulin - blood ; Intercellular Signaling Peptides and Proteins - blood ; Leptin - blood ; Lipids - blood ; lipoproteins ; Male ; Mice ; Mice, Inbred C57BL ; obesity ; Obesity - blood ; Obesity - drug therapy ; Piperidines - therapeutic use ; Pyrazoles - therapeutic use ; rimonabant</subject><ispartof>Diabetes, obesity & metabolism, 2005-01, Vol.7 (1), p.65-72</ispartof><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4044-30b89fd411770f642bb5d5f3f78c9e6b4fe00540d5df0b0387aa120131c997a23</citedby><cites>FETCH-LOGICAL-c4044-30b89fd411770f642bb5d5f3f78c9e6b4fe00540d5df0b0387aa120131c997a23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1463-1326.2004.00374.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1463-1326.2004.00374.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15642077$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Poirier, B.</creatorcontrib><creatorcontrib>Bidouard, J.-P.</creatorcontrib><creatorcontrib>Cadrouvele, C.</creatorcontrib><creatorcontrib>Marniquet, X.</creatorcontrib><creatorcontrib>Staels, B.</creatorcontrib><creatorcontrib>O'Connor, S. E.</creatorcontrib><creatorcontrib>Janiak, P.</creatorcontrib><creatorcontrib>Herbert, J.-M.</creatorcontrib><title>The anti-obesity effect of rimonabant is associated with an improved serum lipid profile</title><title>Diabetes, obesity & metabolism</title><addtitle>Diabetes Obes Metab</addtitle><description>We investigated the effects of chronic treatment with the CB1 receptor antagonist rimonabant (10 mg/kg/day p.o. for 10 weeks) in mice with established obesity (5‐month high‐fat diet). Untreated obese mice showed a weight gain of 46% (45.0 ± 0.6 g vs. 30.8 ± 0.5 g) compared with age‐matched animals fed a standard diet. Rimonabant treatment, commencing after 5‐month high‐fat diet, produced a marked and sustained decrease in body weight (34.5 ± 0.8 g vs. 47.2 ± 0.5 g in the high‐fat vehicle group, p < 0.001). The anti‐obesity effect of rimonabant was similar to that obtained by switching obese mice from high‐fat diet to standard laboratory diet during 10 weeks (final weight 33.7 ± 0.6 g) and was associated with only transient (14 days) reduction in energy intake. Serum leptin, insulin and glucose levels were markedly elevated in obese animals. Rimonabant treatment significantly reduced these elevations (leptin −81%, insulin −78%, glucose −67%, p < 0.001 in all cases vs. high‐fat vehicle group). In addition, rimonabant treatment modestly but significantly increased serum adiponectin levels (+18%, p < 0.05 vs. high‐fat vehicle group). Obese mice demonstrated abnormal serum lipid profiles. Although rimonabant did not modify high‐density lipoprotein cholesterol (HDLc) and had modest effects on total cholesterol, it significantly reduced triglycerides and low‐density lipoprotein cholesterol (LDLc) and, notably, increased the HDLc/LDLc ratio (12.4 ± 0.8 vs. 7.9 ± 0.2 in high‐fat vehicle group, p < 0.001). Therefore, in a model of established obesity, chronic rimonabant treatment produces a marked and sustained decrease in body weight (equivalent to that achieved by dietary change) which is associated with favourable modifications in serum biochemical and lipid profiles.</description><subject>Adiponectin</subject><subject>Animals</subject><subject>Anti-Obesity Agents - therapeutic use</subject><subject>Blood Glucose - analysis</subject><subject>body weight</subject><subject>CB1 receptor antagonist</subject><subject>Cholesterol - blood</subject><subject>Cholesterol, HDL - blood</subject><subject>food intake</subject><subject>glucose</subject><subject>insulin</subject><subject>Insulin - blood</subject><subject>Intercellular Signaling Peptides and Proteins - blood</subject><subject>Leptin - blood</subject><subject>Lipids - blood</subject><subject>lipoproteins</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>obesity</subject><subject>Obesity - blood</subject><subject>Obesity - drug therapy</subject><subject>Piperidines - therapeutic use</subject><subject>Pyrazoles - therapeutic use</subject><subject>rimonabant</subject><issn>1462-8902</issn><issn>1463-1326</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkMtOwzAQRS0EolD4BeQVu4Rx7MSJxIYWKEiFbspjZzmJrbokTYkT2v49TluVLd54NHPPPC5CmIBP3LuZ-4RF1CM0iPwAgPkAlDN_fYTODoXjbRx4cQJBD51bOwenpDE_RT0SRiwAzs_Q53SmsFw0xqtSZU2zwUprlTW40rg2ZbWQqatiY7G0tsqMbFSOV6aZOQibcllXPy5hVd2WuDBLk2OX0qZQF-hEy8Kqy_3fR2-PD9PhkzeejJ6Hd2MvY8CYRyGNE50zQjgH7bZK0zAPNdU8zhIVpUwrgJBBHuYaUnDrS0kCIJRkScJlQPvoetfXzf1ulW1EaWymikIuVNVaEXEaJoyDE8Y7YVZX1tZKi6U7UNYbQUB0roq56MwTnXmic1VsXRVrh17tZ7RpqfI_cG-jE9zuBCt3-ebfjcX95MUFDvd2uLGNWh9wWX916_NQfLyOxGjMIB68gxjQX-dmlF8</recordid><startdate>200501</startdate><enddate>200501</enddate><creator>Poirier, B.</creator><creator>Bidouard, J.-P.</creator><creator>Cadrouvele, C.</creator><creator>Marniquet, X.</creator><creator>Staels, B.</creator><creator>O'Connor, S. 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E. ; Janiak, P. ; Herbert, J.-M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4044-30b89fd411770f642bb5d5f3f78c9e6b4fe00540d5df0b0387aa120131c997a23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Adiponectin</topic><topic>Animals</topic><topic>Anti-Obesity Agents - therapeutic use</topic><topic>Blood Glucose - analysis</topic><topic>body weight</topic><topic>CB1 receptor antagonist</topic><topic>Cholesterol - blood</topic><topic>Cholesterol, HDL - blood</topic><topic>food intake</topic><topic>glucose</topic><topic>insulin</topic><topic>Insulin - blood</topic><topic>Intercellular Signaling Peptides and Proteins - blood</topic><topic>Leptin - blood</topic><topic>Lipids - blood</topic><topic>lipoproteins</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>obesity</topic><topic>Obesity - blood</topic><topic>Obesity - drug therapy</topic><topic>Piperidines - therapeutic use</topic><topic>Pyrazoles - therapeutic use</topic><topic>rimonabant</topic><toplevel>online_resources</toplevel><creatorcontrib>Poirier, B.</creatorcontrib><creatorcontrib>Bidouard, J.-P.</creatorcontrib><creatorcontrib>Cadrouvele, C.</creatorcontrib><creatorcontrib>Marniquet, X.</creatorcontrib><creatorcontrib>Staels, B.</creatorcontrib><creatorcontrib>O'Connor, S. E.</creatorcontrib><creatorcontrib>Janiak, P.</creatorcontrib><creatorcontrib>Herbert, J.-M.</creatorcontrib><collection>Istex</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>Diabetes, obesity & metabolism</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Poirier, B.</au><au>Bidouard, J.-P.</au><au>Cadrouvele, C.</au><au>Marniquet, X.</au><au>Staels, B.</au><au>O'Connor, S. E.</au><au>Janiak, P.</au><au>Herbert, J.-M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The anti-obesity effect of rimonabant is associated with an improved serum lipid profile</atitle><jtitle>Diabetes, obesity & metabolism</jtitle><addtitle>Diabetes Obes Metab</addtitle><date>2005-01</date><risdate>2005</risdate><volume>7</volume><issue>1</issue><spage>65</spage><epage>72</epage><pages>65-72</pages><issn>1462-8902</issn><eissn>1463-1326</eissn><abstract>We investigated the effects of chronic treatment with the CB1 receptor antagonist rimonabant (10 mg/kg/day p.o. for 10 weeks) in mice with established obesity (5‐month high‐fat diet). Untreated obese mice showed a weight gain of 46% (45.0 ± 0.6 g vs. 30.8 ± 0.5 g) compared with age‐matched animals fed a standard diet. Rimonabant treatment, commencing after 5‐month high‐fat diet, produced a marked and sustained decrease in body weight (34.5 ± 0.8 g vs. 47.2 ± 0.5 g in the high‐fat vehicle group, p < 0.001). The anti‐obesity effect of rimonabant was similar to that obtained by switching obese mice from high‐fat diet to standard laboratory diet during 10 weeks (final weight 33.7 ± 0.6 g) and was associated with only transient (14 days) reduction in energy intake. Serum leptin, insulin and glucose levels were markedly elevated in obese animals. Rimonabant treatment significantly reduced these elevations (leptin −81%, insulin −78%, glucose −67%, p < 0.001 in all cases vs. high‐fat vehicle group). In addition, rimonabant treatment modestly but significantly increased serum adiponectin levels (+18%, p < 0.05 vs. high‐fat vehicle group). Obese mice demonstrated abnormal serum lipid profiles. Although rimonabant did not modify high‐density lipoprotein cholesterol (HDLc) and had modest effects on total cholesterol, it significantly reduced triglycerides and low‐density lipoprotein cholesterol (LDLc) and, notably, increased the HDLc/LDLc ratio (12.4 ± 0.8 vs. 7.9 ± 0.2 in high‐fat vehicle group, p < 0.001). Therefore, in a model of established obesity, chronic rimonabant treatment produces a marked and sustained decrease in body weight (equivalent to that achieved by dietary change) which is associated with favourable modifications in serum biochemical and lipid profiles.</abstract><cop>Oxford, UK; Malden, USA</cop><pub>Blackwell Science Ltd</pub><pmid>15642077</pmid><doi>10.1111/j.1463-1326.2004.00374.x</doi><tpages>8</tpages></addata></record> |
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subjects | Adiponectin Animals Anti-Obesity Agents - therapeutic use Blood Glucose - analysis body weight CB1 receptor antagonist Cholesterol - blood Cholesterol, HDL - blood food intake glucose insulin Insulin - blood Intercellular Signaling Peptides and Proteins - blood Leptin - blood Lipids - blood lipoproteins Male Mice Mice, Inbred C57BL obesity Obesity - blood Obesity - drug therapy Piperidines - therapeutic use Pyrazoles - therapeutic use rimonabant |
title | The anti-obesity effect of rimonabant is associated with an improved serum lipid profile |
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