Review Article

The Critical Role of Oxidative Stress in Sarcopenic Obesity

Figure 1

Pathophysiology and consequences of sarcopenic obesity. Sarcopenic obesity (SO) is a combination of obesity and sarcopenia in older people. Obesity and sarcopenia share pathological alterations such as insulin resistance, increased proinflammatory cytokines, age-associated hormonal changes, decreased physical activity, oxidative stress, and liver, adipose, and skeletal muscle dysfunction. Increased body fat mass, especially in the abdominal area (visceral fat), is characteristic of obesity and aging and produces an accumulation of adipose tissue in the liver (liver steatosis) and skeletal muscle (myosteatosis), with the consequent induction of IR, lipotoxicity (Lptx), inflammation, and oxidative stress (Os). Adipocyte hypertrophy induces a state of chronic systemic inflammation characterized by decreased adiponectin and elevated levels of C-reactive protein (CRP), leptin, tumor necrosis factor-α (TNF-α), and interleukin 6 (IL-6). Also, obesity and aging produce hormonal changes such as a decrease in growth hormone (GH), testosterone, estrogen, IGF-1, and adiponectin and an increase in myostatin. Finally, physical inactivity is a common feature of obesity and aging, affecting respiratory, osteoarticular, and neuromuscular levels, inducing loss of physical function. The consequences of sarcopenic obesity are a high risk of fractures, frailty, hospitalization, morbidity and mortality, loss of independence, and decreased quality of life. Abbreviations: SO: sarcopenic obesity; Lptx: lipotoxicity; Os: oxidative stress; CRP: C-reactive protein; TNF-α: tumor necrosis factor-α; IL-6: interleukin 6; GH: growth hormone; IGF-1: insulin-like growth factor 1.