A diagnostic proposal for sarcopenic obesity in adults based on body composition phenotypes.

BACKGROUND & AIMS: Sarcopenic obesity (SO) associates a decrease in lean body mass (LBM) with an excessive increase in fat mass (FM). A number of diagnostic methods, definitions criteria, and thresholds have been proposed for SO resulting in markedly discordant prevalence estimates in populations with obesity. In this study, we first assessed several previously described SO diagnostic criteria and their limitations, and then we propose an innovative approach for identifying SO. METHODS: Data were from a cross-sectional study of a cohort of overweight/obese patients who underwent clinical, laboratory, and body composition assessments by dual-energy X-ray absorptiometry (DXA). We performed unsupervised machine learning through clustering analysis to discriminate lean and fat compartments, and multivariate logistic regressions which provided prognostic variables applied on sex-specific models for SO diagnosis evaluation based on a training dataset (80% of total sample, n = 1165). The predicted models were validated by random forest (RF) machine learning algorithm in the validation dataset (20% of total sample, n = 262). RESULTS: Data from 1427 subjects were analyzed, 79.8% women, mean (±s.d.) age 45.0 (±12.9) years, grade III obesity (BMI over 40 kg/m2) in 42.7%, diabetes in 20.7%, dyslipidemia in 86.3%, and arterial hypertension in 30.3%. Patients with grade III obesity had higher amounts of LBM, FM, and bone mass than subjects with overweight (BMI between 25.0 and 29.9 kg/m2) (p-values < 0.001). When published definitions of SO were applied to this cohort, the prevalence ranged from 0.6% to 96.6%. We built a model that identified 62 (4.3%) individuals as SO, 1125 (78.9%) as non-SO, and 240 (16.8%) as borderline-SO. SO patients showed higher body weight, FM, bone mass, leptin levels, and hepatic steatosis index, but lower LBM and all muscle indexes than non-SO subjects (p-values ≤ 0.001). Patients in the SO and borderline-SO categories were more often females than males (4.5% vs. 3.8% and 16.9% vs. 16.7% respectively, p-value < 0.001) and had significantly higher prevalence of metabolic syndrome and hypertension than non-SO subjects. Males with SO also had higher cardiovascular risk score, while females had higher prevalence of respiratory disorders (p-values < 0.05 for all). CONCLUSIONS: Current diagnostic criteria for SO result in widely discrepant prevalence values leading to diagnosis uncertainty. We developed and validated diagnostic criteria based on body composition phenotypes, specifically for overweight/obese subjects, which identified patients at risk of cardio-metabolic complications. This approach may improve the identification of sarcopenia in subjects with obesity.

Impact of Sarcopenia on the Severity of the Liver Damage in Patients With Non-alcoholic Fatty Liver Disease.

An extensive body of the literature shows a strong interrelationship between the pathogenic pathways of non-alcoholic fatty liver disease (NAFLD) and sarcopenia through the muscle-liver-adipose tissue axis. NAFLD is one of the leading causes of chronic liver diseases (CLD) affecting more than one-quarter of the general population worldwide. The disease severity spectrum ranges from simple steatosis to non-alcoholic steatohepatitis (NASH), cirrhosis, and its complications: end-stage chronic liver disease and hepatocellular carcinoma. Sarcopenia, defined as a progressive loss of the skeletal muscle mass, reduces physical performances, is associated with metabolic dysfunction and, possibly, has a causative role in NAFLD pathogenesis. Muscle mass is a key determinant of the whole-body insulin-mediated glucose metabolism and impacts fatty liver oxidation and energy homeostasis. These mechanisms drive the accumulation of ectopic fat both in the liver (steatosis, fatty liver) and in the muscle (myosteatosis). Myosteatosis rather than the muscle mass per se, seems to be closely associated with the severity of the liver injury. Sarcopenic obesity is a recently described entity which associates both sarcopenia and obesity and may trigger worse clinical outcomes including hepatic fibrosis progression and musculoskeletal disabilities. Furthermore, the muscle-liver-adipose tissue axis has a pivotal role in changes of the body composition, resulting in a distinct clinical phenotype that enables the identification of the "sarcopenic NAFLD phenotype." This review aims to bring some light into the complex relationship between sarcopenia and NAFLD and critically discuss the key mechanisms linking NAFLD to sarcopenia, as well as some of the clinical consequences associated with the coexistence of these two entities: the impact of body composition phenotypes on muscle morphology, the concept of sarcopenic obesity, the relationship between sarcopenia and the severity of the liver damage and finally, the future directions and the existing gaps in the knowledge.