Metabolic syndrome in children and adolescents: definitions, epidemiology, pathophysiology, interventions, and challenges

Abstract

Metabolic syndrome (MetS) is a group of cardiometabolic risk factors with high prevalence in the adult population. To date, there is no consensus on the definition for MetS in children and adolescents despite the presence of well-established diagnostic criteria in adults. The etiology of MetS is associated with a complex interaction between genetic susceptibility and environmental factors, in which the modifiable environmental risk factors are considered to play an important role in this process. MetS is significantly associated with an increased risk of diabetes mellitus and cardiovascular diseases (CVDs). Thus, it is necessary to pay attention to the prevention of MetS in childhood and adulthood. Given the current epidemic of obesity in children and adolescents, there is an urgent need to provide adequate guidelines for the definition, screening, and treatment strategies of MetS in younger patients. In this narrative review, we provide some diagnostic criteria and epidemiological studies and highlight the pathogenesis and management of MetS.

Keywords: adolescents; cardiovascular diseases; children; diabetes mellitus; epidemiology; metabolic syndrome; obesity.

Figure 1

The MetS developmental process: a path diagram from etiology to disease outcome.

Figure 2

MetS pathogenesis in children and adolescents. This figure describes the potential risk factors and mechanisms underlying the pathophysiology of MetS in pediatric populations. Genetic susceptibility and unhealthy lifestyles contribute to central obesity, leading to an imbalance between “aggressive” adipokines produced by adipose tissue and macrophages and the dysfunction of “defensive” adipokines. This imbalance increases immune-inflammatory responses and promotes obesity-related metabolic disorders. The activation of adipose tissue leads to the production of angiotensin II (Ang II) peptides through angiotensin-converting enzyme (ACE), increasing OS and upregulating the expression of lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1), inducing endothelial dysfunction. Additionally, the increased secretion of FFAs from adipose tissue leads to reduced sensitivity in insulin-responsive organs. This cascade ultimately results in IR, dyslipidemia, and hypertension, significantly increasing the risk of MetS, T2DM, and CVD.