Childhood obesity has emerged as a major global health challenge, with a marked increase in prevalence. Defined by excessive fat accumulation, it is associated with an increased risk of developing metabolic syndrome (MetS) and metabolic dysfunction-associated steatotic liver disease (MASLD). These conditions share common pathophysiological mechanisms, involving chronic low-grade inflammation, adipose tissue dysfunction, and insulin resistance. Excess weight contributes to the development of MetS even in the pediatric population through abdominal fat accumulation, dyslipidemia, hypertension, and hyperglycemia, while also creating a pro-inflammatory state that enhances hepatic fat accumulation, leading to MASLD. It is a bidirectional relationship, with MASLD increasing the risk of hypertension and the development of MetS individual components and as a whole. Adipose tissue, especially visceral fat, acts as a metabolic and immunologic organ, producing pro-inflammatory cytokines, which further accentuate insulin resistance and hepatic injury. The “three-strike” hypothesis illustrates the progression of MASLD. Several inflammatory biomarkers, including C-reactive protein, interleukins, adipokines, and serum ferritin, have been studied to monitor and predict disease progression in pediatrics. However, their diagnostic value in children remains limited due to age-related variability and lack of standardized pediatric cut-off points. A unified definition of pediatric MetS and MASLD is crucial to improve study comparability and clinical applicability. Such standardization would support the development of targeted strategies for early identification and intervention.
Podeanu et al. (Wed,) studied this question.