Abstract

The metabolic syndrome defines the clustering of cardiovascular risk factors and is a driven by peripheral insulin resistance. The 'driving force' of the syndrome, i.e. insulin resistance, develops mainly in obese children due to a specific pattern of lipid partitioning characterized by increased deposition of fat in the visceral compartment as well as in insulin-responsive tissues, such as muscle and liver. Such a lipid deposition pattern results in peripheral insulin resistance and a compensatory hyperinsulinemia. Hyperinsulinemia results in normal response of tissues and metabolic pathways that maintained their insulin sensitivity, leading to the typical biochemical and clinical manifestations of the metabolic syndrome. The definition of the syndrome in childhood suffers from many limitations related to different ethnic characteristics as well as age and development dependency of some of the components. Despite these limitations, the clustering of risk factors characteristic of the syndrome in childhood is associated with accelerated atherogenesis in adulthood. Thus, using threshold-based definitions of the syndrome is still important, useful and practical for the sake of risk stratification, longitudinal follow-up and potentially for treatment considerations.

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