Telmisartan increases fatty acid oxidation in skeletal muscle through a peroxisome proliferator-activated receptor-γ dependent pathway
OBJECTIVESTelmisartan is an angiotensin II receptor blocker and selective modulator of peroxisome proliferator-activated receptor-γ reported to increase energy expenditure and improve glucose and lipid metabolism compared with other angiotensin II receptor blockers. As muscle fatty acid oxidation is...
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| Veröffentlicht in: | Journal of hypertension 2008-06, Vol.26 (6), p.1209-1215 |
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| creator | Sugimoto, Ken Kazdová, Ludmila Qi, Nathan R Hyakukoku, Masaya Křen, Vladimír Šimáková, Miroslava Zídek, Václav Kurtz, Theodore W Pravenec, Michal |
| description | OBJECTIVESTelmisartan is an angiotensin II receptor blocker and selective modulator of peroxisome proliferator-activated receptor-γ reported to increase energy expenditure and improve glucose and lipid metabolism compared with other angiotensin II receptor blockers. As muscle fatty acid oxidation is a major determinant of energy expenditure, we investigated the effects of telmisartan on skeletal muscle fatty acid oxidation in a rat model of the metabolic syndrome.
METHODSWe measured fatty acid oxidation in soleus muscles obtained from polydactylous (PD)/Cub rats fed a high sucrose, high fat diet and treated with either telmisartan or losartan. In addition, we measured fatty acid oxidation in soleus muscle tissue isolated from Sprague–Dawley rats, incubated for 3 h with either telmisartan or valsartan.
RESULTSCompared with treatment with losartan, treatment with telmisartan was associated with significantly greater palmitate oxidation in skeletal muscle (44.4 ± 2.9 versus 28.9 ± 3.2 nmol palmitate/g/2 h, P = 0.004) as well as significantly greater glucose tolerance and significantly lower body weight and visceral adiposity. In addition, in-vitro incubation of skeletal muscle with telmisartan induced significantly greater increase in palmitate oxidation than in-vitro incubation with valsartan (9.4 ± 1.6 versus 0.2 ± 4.3 nmol palmitate/g/h, P < 0.05). The increased fatty acid oxidation induced by telmisartan in vitro was blocked by addition of the peroxisome proliferator-activated receptor-γ antagonist GW9662 (−0.4 ± 1.8 nmol palmitate/g/h, P < 0.05).
CONCLUSIONThe current results are consistent with the possibility that telmisartan may increase energy expenditure and protect against dietary induced obesity and features of the metabolic syndrome at least in part by increasing muscle fatty acid oxidation through activation of peroxisome proliferator-activated receptor-γ. |
| doi_str_mv | 10.1097/HJH.0b013e3282f9b58a |
| format | Article |
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METHODSWe measured fatty acid oxidation in soleus muscles obtained from polydactylous (PD)/Cub rats fed a high sucrose, high fat diet and treated with either telmisartan or losartan. In addition, we measured fatty acid oxidation in soleus muscle tissue isolated from Sprague–Dawley rats, incubated for 3 h with either telmisartan or valsartan.
RESULTSCompared with treatment with losartan, treatment with telmisartan was associated with significantly greater palmitate oxidation in skeletal muscle (44.4 ± 2.9 versus 28.9 ± 3.2 nmol palmitate/g/2 h, P = 0.004) as well as significantly greater glucose tolerance and significantly lower body weight and visceral adiposity. In addition, in-vitro incubation of skeletal muscle with telmisartan induced significantly greater increase in palmitate oxidation than in-vitro incubation with valsartan (9.4 ± 1.6 versus 0.2 ± 4.3 nmol palmitate/g/h, P < 0.05). The increased fatty acid oxidation induced by telmisartan in vitro was blocked by addition of the peroxisome proliferator-activated receptor-γ antagonist GW9662 (−0.4 ± 1.8 nmol palmitate/g/h, P < 0.05).
CONCLUSIONThe current results are consistent with the possibility that telmisartan may increase energy expenditure and protect against dietary induced obesity and features of the metabolic syndrome at least in part by increasing muscle fatty acid oxidation through activation of peroxisome proliferator-activated receptor-γ.</description><identifier>ISSN: 0263-6352</identifier><identifier>EISSN: 1473-5598</identifier><identifier>DOI: 10.1097/HJH.0b013e3282f9b58a</identifier><identifier>PMID: 18475159</identifier><identifier>CODEN: JOHYD3</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins, Inc</publisher><subject>Adiposity - drug effects ; Angiotensin II Type 1 Receptor Blockers - pharmacology ; Animals ; Arterial hypertension. Arterial hypotension ; Benzimidazoles - pharmacology ; Benzoates - pharmacology ; Biological and medical sciences ; Blood and lymphatic vessels ; Blood vessels and receptors ; Cardiology. Vascular system ; Fatty Acids - metabolism ; Fundamental and applied biological sciences. Psychology ; Losartan - pharmacology ; Male ; Medical sciences ; Muscle, Skeletal - metabolism ; Oxidation-Reduction ; PPAR gamma - metabolism ; Rats ; Rats, Sprague-Dawley ; Rats, Wistar ; Vertebrates: cardiovascular system ; Weight Gain - drug effects</subject><ispartof>Journal of hypertension, 2008-06, Vol.26 (6), p.1209-1215</ispartof><rights>2008 Lippincott Williams & Wilkins, Inc.</rights><rights>2008 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3801-833d8c3f4319df179ce601d903475fd608ca742bfc4b116ea18e1c9fcde6b7143</citedby><cites>FETCH-LOGICAL-c3801-833d8c3f4319df179ce601d903475fd608ca742bfc4b116ea18e1c9fcde6b7143</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20329268$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18475159$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sugimoto, Ken</creatorcontrib><creatorcontrib>Kazdová, Ludmila</creatorcontrib><creatorcontrib>Qi, Nathan R</creatorcontrib><creatorcontrib>Hyakukoku, Masaya</creatorcontrib><creatorcontrib>Křen, Vladimír</creatorcontrib><creatorcontrib>Šimáková, Miroslava</creatorcontrib><creatorcontrib>Zídek, Václav</creatorcontrib><creatorcontrib>Kurtz, Theodore W</creatorcontrib><creatorcontrib>Pravenec, Michal</creatorcontrib><title>Telmisartan increases fatty acid oxidation in skeletal muscle through a peroxisome proliferator-activated receptor-γ dependent pathway</title><title>Journal of hypertension</title><addtitle>J Hypertens</addtitle><description>OBJECTIVESTelmisartan is an angiotensin II receptor blocker and selective modulator of peroxisome proliferator-activated receptor-γ reported to increase energy expenditure and improve glucose and lipid metabolism compared with other angiotensin II receptor blockers. As muscle fatty acid oxidation is a major determinant of energy expenditure, we investigated the effects of telmisartan on skeletal muscle fatty acid oxidation in a rat model of the metabolic syndrome.
METHODSWe measured fatty acid oxidation in soleus muscles obtained from polydactylous (PD)/Cub rats fed a high sucrose, high fat diet and treated with either telmisartan or losartan. In addition, we measured fatty acid oxidation in soleus muscle tissue isolated from Sprague–Dawley rats, incubated for 3 h with either telmisartan or valsartan.
RESULTSCompared with treatment with losartan, treatment with telmisartan was associated with significantly greater palmitate oxidation in skeletal muscle (44.4 ± 2.9 versus 28.9 ± 3.2 nmol palmitate/g/2 h, P = 0.004) as well as significantly greater glucose tolerance and significantly lower body weight and visceral adiposity. In addition, in-vitro incubation of skeletal muscle with telmisartan induced significantly greater increase in palmitate oxidation than in-vitro incubation with valsartan (9.4 ± 1.6 versus 0.2 ± 4.3 nmol palmitate/g/h, P < 0.05). The increased fatty acid oxidation induced by telmisartan in vitro was blocked by addition of the peroxisome proliferator-activated receptor-γ antagonist GW9662 (−0.4 ± 1.8 nmol palmitate/g/h, P < 0.05).
CONCLUSIONThe current results are consistent with the possibility that telmisartan may increase energy expenditure and protect against dietary induced obesity and features of the metabolic syndrome at least in part by increasing muscle fatty acid oxidation through activation of peroxisome proliferator-activated receptor-γ.</description><subject>Adiposity - drug effects</subject><subject>Angiotensin II Type 1 Receptor Blockers - pharmacology</subject><subject>Animals</subject><subject>Arterial hypertension. Arterial hypotension</subject><subject>Benzimidazoles - pharmacology</subject><subject>Benzoates - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Blood vessels and receptors</subject><subject>Cardiology. Vascular system</subject><subject>Fatty Acids - metabolism</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Losartan - pharmacology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Muscle, Skeletal - metabolism</subject><subject>Oxidation-Reduction</subject><subject>PPAR gamma - metabolism</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Rats, Wistar</subject><subject>Vertebrates: cardiovascular system</subject><subject>Weight Gain - drug effects</subject><issn>0263-6352</issn><issn>1473-5598</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkU1u1DAUgC0EokPhBgh5A7sU_ySOvUQVdECV2JR19GI_k1BPEmynw5ygB-IenAmPOqISC8uy_b0_f4S85uyCM9O-337ZXrCecYlSaOFN32h4Qja8bmXVNEY_JRsmlKyUbMQZeZHSD8aYNq18Ts64rtuGN2ZD7m8w7MYEMcNEx8lGhISJesj5QMGOjs6_Rgd5nI_PNN1iwAyB7tZkA9I8xHn9PlCgC8ZCpnmHdIlzGD1GyHOswObxDjI6GtHicrz685s6XHByOGW6QB72cHhJnnkICV-d9nPy7dPHm8ttdf316vPlh-vKSs14paV02kpfS26c562xqBh3hskykHeKaQttLXpv655zhcA1cmu8daj6ltfynLx7yFua_Lliyl2Z3mIIMOG8pk4ZwSVXooD1A2jjnFJE3y1x3EE8dJx1RwFdEdD9L6CEvTnlX_sduseg048X4O0JgGQh-AiTHdM_TjApjFD6sf5-Dhljug3rHmM3IIQ8dEUlq3UrKlGcMlVOVVml9b97JaPh</recordid><startdate>200806</startdate><enddate>200806</enddate><creator>Sugimoto, Ken</creator><creator>Kazdová, Ludmila</creator><creator>Qi, Nathan R</creator><creator>Hyakukoku, Masaya</creator><creator>Křen, Vladimír</creator><creator>Šimáková, Miroslava</creator><creator>Zídek, Václav</creator><creator>Kurtz, Theodore W</creator><creator>Pravenec, Michal</creator><general>Lippincott Williams & Wilkins, Inc</general><general>Lippincott Williams & Wilkins</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>7X8</scope></search><sort><creationdate>200806</creationdate><title>Telmisartan increases fatty acid oxidation in skeletal muscle through a peroxisome proliferator-activated receptor-γ dependent pathway</title><author>Sugimoto, Ken ; Kazdová, Ludmila ; Qi, Nathan R ; Hyakukoku, Masaya ; Křen, Vladimír ; Šimáková, Miroslava ; Zídek, Václav ; Kurtz, Theodore W ; Pravenec, Michal</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3801-833d8c3f4319df179ce601d903475fd608ca742bfc4b116ea18e1c9fcde6b7143</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Adiposity - drug effects</topic><topic>Angiotensin II Type 1 Receptor Blockers - pharmacology</topic><topic>Animals</topic><topic>Arterial hypertension. Arterial hypotension</topic><topic>Benzimidazoles - pharmacology</topic><topic>Benzoates - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Blood vessels and receptors</topic><topic>Cardiology. Vascular system</topic><topic>Fatty Acids - metabolism</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Losartan - pharmacology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Muscle, Skeletal - metabolism</topic><topic>Oxidation-Reduction</topic><topic>PPAR gamma - metabolism</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Rats, Wistar</topic><topic>Vertebrates: cardiovascular system</topic><topic>Weight Gain - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sugimoto, Ken</creatorcontrib><creatorcontrib>Kazdová, Ludmila</creatorcontrib><creatorcontrib>Qi, Nathan R</creatorcontrib><creatorcontrib>Hyakukoku, Masaya</creatorcontrib><creatorcontrib>Křen, Vladimír</creatorcontrib><creatorcontrib>Šimáková, Miroslava</creatorcontrib><creatorcontrib>Zídek, Václav</creatorcontrib><creatorcontrib>Kurtz, Theodore W</creatorcontrib><creatorcontrib>Pravenec, Michal</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>MEDLINE - Academic</collection><jtitle>Journal of hypertension</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sugimoto, Ken</au><au>Kazdová, Ludmila</au><au>Qi, Nathan R</au><au>Hyakukoku, Masaya</au><au>Křen, Vladimír</au><au>Šimáková, Miroslava</au><au>Zídek, Václav</au><au>Kurtz, Theodore W</au><au>Pravenec, Michal</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Telmisartan increases fatty acid oxidation in skeletal muscle through a peroxisome proliferator-activated receptor-γ dependent pathway</atitle><jtitle>Journal of hypertension</jtitle><addtitle>J Hypertens</addtitle><date>2008-06</date><risdate>2008</risdate><volume>26</volume><issue>6</issue><spage>1209</spage><epage>1215</epage><pages>1209-1215</pages><issn>0263-6352</issn><eissn>1473-5598</eissn><coden>JOHYD3</coden><abstract>OBJECTIVESTelmisartan is an angiotensin II receptor blocker and selective modulator of peroxisome proliferator-activated receptor-γ reported to increase energy expenditure and improve glucose and lipid metabolism compared with other angiotensin II receptor blockers. As muscle fatty acid oxidation is a major determinant of energy expenditure, we investigated the effects of telmisartan on skeletal muscle fatty acid oxidation in a rat model of the metabolic syndrome.
METHODSWe measured fatty acid oxidation in soleus muscles obtained from polydactylous (PD)/Cub rats fed a high sucrose, high fat diet and treated with either telmisartan or losartan. In addition, we measured fatty acid oxidation in soleus muscle tissue isolated from Sprague–Dawley rats, incubated for 3 h with either telmisartan or valsartan.
RESULTSCompared with treatment with losartan, treatment with telmisartan was associated with significantly greater palmitate oxidation in skeletal muscle (44.4 ± 2.9 versus 28.9 ± 3.2 nmol palmitate/g/2 h, P = 0.004) as well as significantly greater glucose tolerance and significantly lower body weight and visceral adiposity. In addition, in-vitro incubation of skeletal muscle with telmisartan induced significantly greater increase in palmitate oxidation than in-vitro incubation with valsartan (9.4 ± 1.6 versus 0.2 ± 4.3 nmol palmitate/g/h, P < 0.05). The increased fatty acid oxidation induced by telmisartan in vitro was blocked by addition of the peroxisome proliferator-activated receptor-γ antagonist GW9662 (−0.4 ± 1.8 nmol palmitate/g/h, P < 0.05).
CONCLUSIONThe current results are consistent with the possibility that telmisartan may increase energy expenditure and protect against dietary induced obesity and features of the metabolic syndrome at least in part by increasing muscle fatty acid oxidation through activation of peroxisome proliferator-activated receptor-γ.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins, Inc</pub><pmid>18475159</pmid><doi>10.1097/HJH.0b013e3282f9b58a</doi><tpages>7</tpages></addata></record> |
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| source | Journals@Ovid Ovid Autoload; MEDLINE |
| subjects | Adiposity - drug effects Angiotensin II Type 1 Receptor Blockers - pharmacology Animals Arterial hypertension. Arterial hypotension Benzimidazoles - pharmacology Benzoates - pharmacology Biological and medical sciences Blood and lymphatic vessels Blood vessels and receptors Cardiology. Vascular system Fatty Acids - metabolism Fundamental and applied biological sciences. Psychology Losartan - pharmacology Male Medical sciences Muscle, Skeletal - metabolism Oxidation-Reduction PPAR gamma - metabolism Rats Rats, Sprague-Dawley Rats, Wistar Vertebrates: cardiovascular system Weight Gain - drug effects |
| title | Telmisartan increases fatty acid oxidation in skeletal muscle through a peroxisome proliferator-activated receptor-γ dependent pathway |
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