Features of endocrine status in obese children and polymorphisms of the lactase gene
Background. Obesity is an imbalance of immunocytokine and neuroendocrine regulation of energy metabolism with excessive accumulation of adipose tissue in the body accompanied by the formation of a chronic proinflammatory immune response associated with the genotype C/C 13910 of the lactase gene. Childhood obesity is a risk factor for the development of type 2 diabetes, steatohepatosis, cardiovascular diseases, orthopedic problems and mental disorders causing both short-term and long-term adverse effects on physical and psychosocial well-being. Materials and methods. A comprehensive examination was carried out according to the current protocols in the field of pediatric endocrinology for 76 children aged 6 to 18 years with obesity and SNP LCT. The first group (n = 36) was composed of children with genotype С/C 13910, which is associated with adult type of lactase deficiency. The second group (n = 40) presented phenotypically similar children with genotypes C/T and T/T 13910 associated with lactase persistence. The determination of lipid disorders was carried out using bioimpedancemetry on the Tefal Bodysignal electronic scales (France). The study of the endocrine system was performed using an immunochemical test method with electrochemiluminescence immunoassay, genotyping of the lactase gene by real time polymerase chain reaction. Results. Children with genotype C/C 13910 have statistically significant differences in endocrine status associated with an increase in insulin resistance in boys up to 6.79 ± 1.12 in the HOMA index, compared with 3.29 ± 0.99 in boys with C/T and T/T 13910 genotypes; p = 0.028. In girls with the C/C 13910 genotype, there is a relative, within the limits of the physiological norm, decrease in free estradiol to 40.10 ± 0.05 pg/ml, as compared with the level of girls with C/T and T/T 13910 genotypes — 75.61 ± 4.60 pg/ml, p < 0.01, with simultaneous pathological dehydroepiandrosterone sulfate increase by 3.5 times at the age of 15–18 years to 594.50 ± 8.81 μg/dl relative to the level of girls with genotypes C/T and T/T 13910 — 167.0 ± 12.8 μg/dl, p < 0.01. For girls with the genotype C/C 13910, a statistically significant (p < 0.05) increase in the level of leptin to 47.84 ± 4.40 ng/ml is observed, compared with girls with genotypes C/T and T/T 13910 — 32.54 ± 4.30 ng/ml. Malnutrition disorders are associated with a higher body fat mass (BFM) in boys and girls with the C/C 13910 genotype as compared to children with genotypes C/T and T/T 13910, namely, in boys with the genotype C/C 13910, mean BFM level was 35.46 ± 2.52 %, while in boys with C/C and T/T 13910 genotypes — 25.04 ± 2.14 %. For girls with genotype C/C 13910, the mean BFM was 38.19 ± 2.25 %, whereas in girls with genotypes C/T and T/T 13910, the mean BFM was 28.99 ± 0.76 %, with p < 0.001. Conclusions. The risk factor for obesity in children is the lactase gene C/C 13910 genotype, which is associated with adult lactase deficiency. Obese boys aged 6–18 years, carriers of this genotype, have 1.5 times higher risk of developing insulin resistance and type 2 diabetes. Obese girls aged 15–18 years with the C/C 13910 genotype have 1.5 times higher risk of leptin resistance and 3.5 times — the risk of inverted puberty period due to hyperandrogenemia of the adrenal origin, which taken as a whole causes polycystic ovary syndrome, infertility. The obtained data can be used to substantiate the scientific and practical program for optimization of protocols for the diagnosis and treatment of obesity associated with lactase deficiency of an adult type in childhood.
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