Nabil E Boutagy1, Elaina L Marinik1, Ryan P McMillan2, Angela S Anderson1, Madlyn I Frisard3, Brenda M Davy4, Jose M Rivero5, Kevin P Davy3, Matthew W Hulver6. 1. Department of Human Nutrition, Foods, and Exercise, Virginia Tech, Blacksburg, VA, USA. 2. Department of Human Nutrition, Foods, and Exercise, and The Metabolic Phenotyping Core Virginia Tech, Blacksburg, VA, USA. 3. Department of Human Nutrition, Foods, and Exercise, The Metabolic Phenotyping Core and the Fralin Translational Obesity Research Center, Virginia Tech, Blacksburg, VA, USA. 4. Department of Human Nutrition, Foods, and Exercise, and the Fralin Translational Obesity Research Center, Virginia Tech, Blacksburg, VA, USA. 5. Heart Specialists of Southwest Virginia, Christiansburg, VA, USA. 6. Wallace Hall, Room 338A; 295 West Campus Drive Blacksburg, VA 24061, USA hulvermw@vt.edu.
Abstract
OBJECTIVES: Whether angiotensin II receptor blockade improves skeletal muscle fatty acid oxidation in overweight and obese humans is unknown. The purpose of the study was to test the hypothesis that the angiotensin II receptor blocker, olmesartan, would increase fatty acid oxidation and the activity of enzymes associated with oxidative metabolism in skeletal muscle of overweight and obese humans. METHODS: A total of 12 individuals (6 men and 6 women) aged 18-75 and with a body mass index ⩾25 kg/m2 were assigned to olmesartan or placebo for 8 weeks in a crossover fashion. Fatty acid oxidation was measured before and after each intervention by counting the (14)CO2 produced from [1-(14)C] palmitic acid in skeletal muscle homogenates. RESULTS:Fatty acid oxidation was not significantly different between treatment periods at baseline and post intervention. In addition, the enzyme activities of citrate synthase and β-hydroxyacyl-coenzyme A dehydrogenase in skeletal muscle homogenates did not differ between treatment periods at baseline or post intervention. CONCLUSIONS: Treatment with olmesartan for 8 weeks does not improve fatty acid oxidation or the activity of enzymes associated with oxidative metabolism in skeletal muscle from overweight and obese individuals. Taken together, our results indicate that improvements in skeletal muscle metabolism are not among the additional benefits of olmesartan that extend beyond blood pressure reduction.
RCT Entities:
OBJECTIVES: Whether angiotensin II receptor blockade improves skeletal muscle fatty acid oxidation in overweight and obesehumans is unknown. The purpose of the study was to test the hypothesis that the angiotensin II receptor blocker, olmesartan, would increase fatty acid oxidation and the activity of enzymes associated with oxidative metabolism in skeletal muscle of overweight and obesehumans. METHODS: A total of 12 individuals (6 men and 6 women) aged 18-75 and with a body mass index ⩾25 kg/m2 were assigned to olmesartan or placebo for 8 weeks in a crossover fashion. Fatty acid oxidation was measured before and after each intervention by counting the (14)CO2 produced from [1-(14)C] palmitic acid in skeletal muscle homogenates. RESULTS:Fatty acid oxidation was not significantly different between treatment periods at baseline and post intervention. In addition, the enzyme activities of citrate synthase and β-hydroxyacyl-coenzyme A dehydrogenase in skeletal muscle homogenates did not differ between treatment periods at baseline or post intervention. CONCLUSIONS: Treatment with olmesartan for 8 weeks does not improve fatty acid oxidation or the activity of enzymes associated with oxidative metabolism in skeletal muscle from overweight and obese individuals. Taken together, our results indicate that improvements in skeletal muscle metabolism are not among the additional benefits of olmesartan that extend beyond blood pressure reduction.