Changes in depression, anxiety, and post-traumatic stress symptoms among children and adolescents exposed to adverse childhood experiences following participation in the PROACT intervention in Nairobi

Sarcopenic obesity (SO), first proposed by Heber et al. in 1996, is a distinct clinical syndrome characterized by the simultaneous decline in skeletal muscle mass and function accompanied by excessive fat accumulation, rather than the mere coexistence of sarcopenia and obesity (). With the aging global population and the rising prevalence of obesity, SO has emerged as an important clinical health concern and has garnered increasing attention (). Individuals with SO bear a “double burden” of muscle loss and excess adiposity, placing them at higher risk of frailty, falls, functional decline, metabolic dysregulation, and all-cause mortality (), with an estimated 24% higher risk of death compared to non-SO individuals (). Diabetes mellitus is one of the most prevalent chronic non-communicable diseases worldwide, and its prevalence continues to rise. According to projections from the International Diabetes Federation (IDF), the global number of individuals with diabetes is expected to reach 783 million by 2045 (). The interplay between SO and diabetes has been increasingly recognized (). Diabetes provides a metabolic milieu for the development of SO through insulin resistance, chronic low-grade inflammation, hormonal dysregulation, and lipid metabolism abnormalities, thereby accelerating disease progression (). Accumulating evidence suggests that SO is not only highly prevalent in older and metabolically compromised populations but also confers a greater risk of adverse cardiometabolic outcomes, including impaired glucose homeostasis and incident type 2 diabetes, beyond the risk associated with sarcopenia or obesity alone (). This synergistic risk may be driven by the complex crosstalk between adipose tissue and skeletal muscle, wherein dysfunctional adipokine signaling, chronic low-grade inflammation, and insulin resistance disrupt anabolic signaling pathways, leading to impaired muscle protein synthesis and enhanced proteolysis (, ). Evidence indicates that the presence of SO may further increase the risk of type 2 diabetes. This association is likely mediated by reduced muscle mass impairing glucose utilization, while excess adipose tissue activates chronic inflammatory pathways. The resulting muscle loss diminishes glucose uptake, and dysfunctional adipose tissue-muscle crosstalk promotes chronic inflammation and insulin resistance through inflammation and impaired insulin signaling, establishing a self-perpetuating metabolic imbalance (). Although previous studies have reported the prevalence of SO among patients with diabetes, existing evidence indicates an overall prevalence of approximately 27% (). However, the recent literature over the past 3 years has not been systematically synthesized, and associated factors have not been comprehensively analyzed, which limits the ability to identify high-risk populations and inform targeted interventions. Furthermore, previous studies have not fully examined variations in patient sources, diagnostic criteria for SO, or associated factors. Therefore, the present study aims to conduct a systematic review and meta-analysis to comprehensively evaluate the prevalence of SO and factors associated with SO among adults with diabetes across different clinical and community settings, providing evidence for the identification of high-risk populations, optimization of chronic disease management, and development of targeted intervention strategies.