THE ROLE OF PEPTIDE YY3-36 IN THE DEVELOPMENT OF METABOLIC SYNDROME IN CHILDREN WITH OBESITY

Abstract

This article presents data from a study of peptide YY-36 in obese children, which plays a key role in the regulation of eating behavior. This peptide is synthesized by L-cells in the distal small and large intestines, enters circulation after meals, and is an anorexigenic hormone. The results of this study are recommended for widespread implementation in the practice of pediatricians, general practitioners, and pediatric endocrinologists. Study objective: To determine the contribution of peptide YY3-36 to the development of metabolic syndrome in children with obesity. Materials and methods: A total of 108 children with exogenous-constitutional obesity, abdominal fat distribution, and waist circumference greater than the 90th percentile for age and sex were examined. For comparative analysis, 76 children with normal body weight were examined. A comprehensive set of anthropometric, biochemical, and enzyme immunoassay studies was conducted, and serum peptide YY3-36 levels were determined. Based on the criteria for diagnosing metabolic syndrome, the frequency of metabolic syndrome, its various forms, and combinations were determined in children with abdominal obesity. Study results: When studying peptide YY3-36 levels in obese children, a significant decrease was found in children with abdominal obesity (72,13 pg/ml), which was significantly lower than in controls (105,39 pg/ml; p< 0.001). When determining the gender dependence of intestinal neuroregulatory peptide YY3-36 production, statistically lower levels were observed in boys compared to girls, indicating a more pronounced imbalance in peptide YY3-36 production in boys with visceral fat distribution. The study noted a tendency toward decreased YY3-36 peptide levels as children aged 16-18 years compared to children aged 10-15 years. No similar age-related dynamics were observed in children in the control group. The duration of obesity in children with abdominal obesity played a role in the production of intestinal neuroregulatory peptide. YY3-36 peptide levels progressively decreased with increasing duration of the disease, which was apparently associated with a gradually increasing eating disorder. The study demonstrated that all children with abdominal obesity had low YY3-36 peptide levels, indicating an eating disorder, which is one of the dominant factors in the development of metabolic syndrome in the entire sample of children, with the lowest values ​​in children with complete metabolic syndrome. Currently, there is no interpretation of peptide YY3-36 levels for diagnosing pathological conditions, including metabolic syndrome, in children with obesity. Therefore, a threshold level for peptide YY3-36 was determined to assess the contribution of this hormone to the diagnosis of metabolic syndrome in children with abdominal obesity. In a study of the AUC-ROC of peptide YY3-36 levels, the AUC curve area reached sufficient diagnostic values at a threshold level ≤71,600, with a sensitivity of 84.2% and a specificity of 73.4%, demonstrating the good diagnostic accuracy of the AUC-ROC test (AUC = 0,856). Conclusions: The study suggests a significant contribution of abnormal peptide YY3-36 production to the development of abdominal obesity in children. The conducted work characterizes a significant decrease in the production of this food hormone in metabolic syndrome in children, the degree of pathology of which was greatest in boys with the full form of the syndrome.