['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.', '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.', '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).'] Does telmisartan increase fatty acid oxidation in skeletal muscle through a peroxisome proliferator-activated receptor-gamma dependent pathway?