The epidemic of childhood obesity has been shown to be the key determinant of the co-occurrence in childhood of several metabolic abnormalities including hypertension, dyslipidemia, insulin resistance and impaired glucose tolerance. This cluster of abnormalities is defined as metabolic syndrome (MetS), a disorder once mainly found in adults, and associated with an increased incidence of several non-communicable diseases (NCD), such as cardiovascular disease, type 2 diabetes and a higher incidence of all-cause mortality during adulthood.
In obese children and adolescents, increased adipose tissue storage characteristically induced a general resistance to the insulin effect only on carbohydrates metabolism, commonly defined as insulin resistance. This dysmetabolic state has been recognized as the key factor in the pathogenesis of metabolic syndrome, both in adults and children. The major cause of insulin resistance in childhood is a typical lipid partitioning pattern characterized by increased deposition of lipids within insulin responsive tissues, such as the liver and skeletal muscle and within the viscera. Although obesity is the most frequent cause of insulin resistance in youths, it should be taken into consideration that a transient physiological insulin-resistant state occurs in children during puberty, maybe due to the increase in growth hormone and sex steroids, and that this state may worsen the insulin resistance present in obese children accelerating the progression to metabolic syndrome and type 2 diabetes.
Although, the definition of metabolic syndrome in adulthood is well established and accepted worldwide, the debate is still open in children and the definition in the pediatric age group is controversial, less stable over time and is harder to utilize clinically. Especially, a lively debate have been reported on the opportunity of an early diagnosis of metabolic syndrome in youth. These contrasts are mainly determined by several reasons and especially by the peculiarity of body proportions changes in growing children, by the determinant role of several pubertal related hormones on some of the criteria defining the syndrome and by a different balance of the factors governing glucose metabolism between obese children and adolescents compared to obese adults.
In addition, during the last decades the liver has been shown to be a key component of this dysmetabolic state affecting the development and co-occurrance of this complex cluster metabolic abnormalities.
Thus, the key points to understand the progression leading to the occurrence of metabolic syndrome and type 2 diabetes are when and how insulin resistance occurs in obese children and adolescents and what are the underlying putative defects leading to glucose dysregulation.
A better understanding of the mechanisms underlying the pathogenesis of insulin resistance and type 2 diabetes in youth is needed. In addition, while environmental factors associated with obesity development are playing a role, it is also important to note that genetic factors may be critical. A complete characterization of the complex mechanisms associated to the risk of metabolic syndrome is necessary in order to open new perspective in the primary and secondary prevention of this dysmetabolic state and especially on its long-term metabolic and cardiovascular consequences.
The epidemic of childhood obesity has been shown to be the key determinant of the co-occurrence in childhood of several metabolic abnormalities including hypertension, dyslipidemia, insulin resistance and impaired glucose tolerance. This cluster of abnormalities is defined as metabolic syndrome (MetS), a disorder once mainly found in adults, and associated with an increased incidence of several non-communicable diseases (NCD), such as cardiovascular disease, type 2 diabetes and a higher incidence of all-cause mortality during adulthood.
In obese children and adolescents, increased adipose tissue storage characteristically induced a general resistance to the insulin effect only on carbohydrates metabolism, commonly defined as insulin resistance. This dysmetabolic state has been recognized as the key factor in the pathogenesis of metabolic syndrome, both in adults and children. The major cause of insulin resistance in childhood is a typical lipid partitioning pattern characterized by increased deposition of lipids within insulin responsive tissues, such as the liver and skeletal muscle and within the viscera. Although obesity is the most frequent cause of insulin resistance in youths, it should be taken into consideration that a transient physiological insulin-resistant state occurs in children during puberty, maybe due to the increase in growth hormone and sex steroids, and that this state may worsen the insulin resistance present in obese children accelerating the progression to metabolic syndrome and type 2 diabetes.
Although, the definition of metabolic syndrome in adulthood is well established and accepted worldwide, the debate is still open in children and the definition in the pediatric age group is controversial, less stable over time and is harder to utilize clinically. Especially, a lively debate have been reported on the opportunity of an early diagnosis of metabolic syndrome in youth. These contrasts are mainly determined by several reasons and especially by the peculiarity of body proportions changes in growing children, by the determinant role of several pubertal related hormones on some of the criteria defining the syndrome and by a different balance of the factors governing glucose metabolism between obese children and adolescents compared to obese adults.
In addition, during the last decades the liver has been shown to be a key component of this dysmetabolic state affecting the development and co-occurrance of this complex cluster metabolic abnormalities.
Thus, the key points to understand the progression leading to the occurrence of metabolic syndrome and type 2 diabetes are when and how insulin resistance occurs in obese children and adolescents and what are the underlying putative defects leading to glucose dysregulation.
A better understanding of the mechanisms underlying the pathogenesis of insulin resistance and type 2 diabetes in youth is needed. In addition, while environmental factors associated with obesity development are playing a role, it is also important to note that genetic factors may be critical. A complete characterization of the complex mechanisms associated to the risk of metabolic syndrome is necessary in order to open new perspective in the primary and secondary prevention of this dysmetabolic state and especially on its long-term metabolic and cardiovascular consequences.
