Document Detail


Telmisartan increases fatty acid oxidation in skeletal muscle through a peroxisome proliferator-activated receptor-gamma dependent pathway.
MedLine Citation:
PMID:  18475159     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVES: Telmisartan is an angiotensin II receptor blocker and selective modulator of peroxisome proliferator-activated receptor-gamma 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.
METHODS: We 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.
RESULTS: Compared 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-gamma antagonist GW9662 (-0.4 +/- 1.8 nmol palmitate/g/h, P < 0.05).
CONCLUSION: The 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-gamma.
Authors:
Ken Sugimoto; Ludmila Kazdová; Nathan R Qi; Masaya Hyakukoku; Vladimír Kren; Miroslava Simáková; Václav Zídek; Theodore W Kurtz; Michal Pravenec
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of hypertension     Volume:  26     ISSN:  0263-6352     ISO Abbreviation:  J. Hypertens.     Publication Date:  2008 Jun 
Date Detail:
Created Date:  2008-05-13     Completed Date:  2008-07-29     Revised Date:  2014-01-09    
Medline Journal Info:
Nlm Unique ID:  8306882     Medline TA:  J Hypertens     Country:  England    
Other Details:
Languages:  eng     Pagination:  1209-15     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Adiposity / drug effects
Angiotensin II Type 1 Receptor Blockers / pharmacology*
Animals
Benzimidazoles / pharmacology*
Benzoates / pharmacology*
Fatty Acids / metabolism*
Losartan / pharmacology
Male
Muscle, Skeletal / metabolism*
Oxidation-Reduction
PPAR gamma / metabolism*
Rats
Rats, Sprague-Dawley
Rats, Wistar
Weight Gain / drug effects
Grant Support
ID/Acronym/Agency:
HL35018/HL/NHLBI NIH HHS; HL56028/HL/NHLBI NIH HHS; HL63709/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Angiotensin II Type 1 Receptor Blockers; 0/Benzimidazoles; 0/Benzoates; 0/Fatty Acids; 0/PPAR gamma; JMS50MPO89/Losartan; U5SYW473RQ/telmisartan

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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