Involvement of oxidative stress in atherosclerosis development in subjects with sarcopenic obesity

Co‐existing decreased muscle mass and increased visceral fat, an age‐associated change called sarcopenic obesity, results in fragility and cardiovascular disease. To assess the pathogenesis of sarcopenic obesity, we assessed the associations of clinical parameters with psoas muscle mass in elderly male subjects with obesity and type 2 diabetes.The subjects were 55 patients, over 65 years of age and with a visceral fat area exceeding 100 cm2, with type 2 diabetes. The cross‐sectional area of the psoas muscle is considered to provide an estimation of overall muscle mass. Sarcopenia was considered to be present when the total psoas muscle area was low, defined as a value below 500 mm2 m−2 on a computed tomographic scan.The maximum intima‐media thickness (max IMT) and urinary 8‐isoprostane values were significantly higher in the sarcopenic group. Multiple linear regression analysis revealed max IMT to be an independent variable related to muscle mass decline. In addition, logistic analysis showed max IMT and urinary 8‐isoprostane to be variables independently contributing to total psoas muscle area <500 mm2 m−2.Worsening surrogate markers for systemic oxidative stress and atherosclerosis were associated with declining muscle mass in elderly subjects with obesity and type 2 diabetes. These results indicate that systemic oxidative stress is among the mechanisms underlying atherosclerosis development in subjects with sarcopenic obesity.