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Angiotensin II receptor blockade and skeletal muscle metabolism in overweight and obese adults with elevated blood pressure

机译:血压升高的超重和肥胖成年人的血管紧张素II受体阻滞和骨骼肌代谢

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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. 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 14CO2 produced from [1-14C] palmitic acid in skeletal muscle homogenates. 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. 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.
机译:血管紧张素II受体阻滞剂是否能改善超重和肥胖人群的骨骼肌脂肪酸氧化尚不清楚。该研究的目的是检验以下假设:血管紧张素II受体阻滞剂奥美沙坦会增加超重和肥胖人骨骼肌中的脂肪酸氧化以及与氧化代谢相关的酶的活性。共有12名年龄在18-75岁且体重指数≤25kg / m2的个体(6名男性和6名女性)被分配给奥美沙坦或安慰剂,进行8周交叉治疗。在每次干预之前和之后,通过计算骨骼肌匀浆中[1-14C]棕榈酸产生的14CO2来测量脂肪酸氧化。在基线和干预后的治疗期间,脂肪酸氧化没有显着差异。另外,在基线或干预后各治疗期之间,骨骼肌匀浆中柠檬酸合酶和β-羟酰基辅酶A脱氢酶的酶活性没有差异。用奥美沙坦治疗8周不能改善超重和肥胖个体骨骼肌中的脂肪酸氧化或与氧化代谢相关的酶的活性。综上所述,我们的结果表明,骨骼肌代谢的改善不是奥美沙坦的其他好处,它不仅可以降低血压。

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