Sarcopenic Obesity: Time to Meet the Challenge

Abstract

The prevalence of overweight and obesity has reached epidemic proportions worldwide due to increasingly pervasive obesogenic lifestyle changes. Obesity poses unprecedented individual, social, and multidisciplinary medical challenges by increasing the risk for metabolic diseases, chronic organ failures, and cancer as well as complication rates in the presence of acute disease conditions. Whereas reducing excess adiposity remains the fundamental pathogenic treatment for obese individuals, complex metabolic and lifestyle abnormalities as well as weight reduction therapies per se may also compromise the ability to preserve muscle function and mass, especially when chronic disease co-exists with obesity. Emerging evidence indicates that low muscle mass and quality have a strong negative prognostic impact in obese individuals and may lead to frailty, disability, and increased morbidity and mortality. Awareness of the importance of skeletal muscle maintenance in obesity is however low among clinicians and scientists. The term ‘sarcopenic obesity' has been proposed to identify obesity with low skeletal muscle function and mass, but its utilization is largely limited to the aging patient population, and consensus on its definition and diagnostic criteria remains insufficient. Knowledge on prevalence of sarcopenic obesity in various clinical conditions and patient subgroups, on its clinical impacts in patient risk stratification, and on effective prevention and treatment strategies remain therefore dramatically inadequate. In particular, optimal dietary options and medical nutritional support strategies to preserve muscle mass in obese individuals remain largely undefined. The European Society for Clinical Nutrition and Metabolism (ESPEN) and the European Association for the Study of Obesity (EASO) recognize and indicate obesity with altered body composition due to low skeletal muscle function and mass (sarcopenic obesity) as a scientific and clinical priority for researchers and clinicians. ESPEN and EASO therefore call for coordinated action aimed at reaching consensus on its definition, diagnostic criteria, and optimal treatment with particular regard to nutritional therapy. We are convinced that achievement of these goals has a strong potential to reduce the burden of morbidity and mortality in the rapidly increasing obese patient population.

Obesity and ageing: Two sides of the same coin

“…With obesity, deleterious alterations in skeletal muscle structure and metabolism may result in declines in muscle mass and function. 154 A common belief is that patients with obesity generate larger muscular force because of the chronic overload stimulus on weight-bearing muscles. However, the body-mass normalized muscular force of patients with obesity is weaker than that of individuals with healthy body weight.…”

Phenotypes of Sarcopenic Obesity: Exploring the Effects on Peri-Muscular Fat, the Obesity Paradox, Hormone-Related Responses and the Clinical Implications

“…Furthermore, with aging, increased levels of leptin, an adipocyte hormone, may result in leptin resistance and a reduction of fatty acid oxidation in muscles which contributes to ectopic fat deposition in skeletal muscle and other tissues leading to muscle atrophy [16]. Other metabolic abnormalities have been described such as mitochondrial dysfunction, muscle oxidative stress and muscle stem cell dysfunction [17].…”

“…This means that obesity in older age does not protect from chronic disease-related mortality when it is associated with sarcopenia. The few available studies indeed indicate that low muscle function and mass may be associated with higher mortality in obese individuals with chronic diseases [17].…”

Effect of Swimming Training and Crocin Consumption on Intrinsic Apoptosis Pathway in Muscle Tissue of High-Fat Diet-induced Obese Rats

“…Studies have shown that obesity is closely related to the development of diseases such as cardiovascular disease, cognitive impairment, cancer, motor disorders, and muscle mass loss (2,3). Evidence also suggests that hyperglycemia is associated with elevated fat mass, leading to increased oxidative stressors, increased pro-inflammatory factors, mitochondrial dysfunction, and ultimately cell death (4). Previous studies have shown the role of the mitochondrial pathway as one of the planned death pathways.…”