Features of endocrine status in obese children and polymorphisms of the lactase gene

A.A. Nikulina

Abstract


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.


Keywords


obesity; children; endocrine status; polymorphisms of the lactase gene

References


Abaturov АЕ, Nikulina AА. Association one-nucleotide polimorphism of the lactase gene in accordance with the insulin resistance of children. Suchasni medychni tehnologii'. 2016;4(31):33-36. (in Ukrainian).

Abaturov AE, Nikulina AА. Association of lactase gene polymorphism with dyslipoproteidemia in children with obesity. Sovremennaya pediatriya. 2017;2(82):118-121. doi: 10.15574/SP.2017.82.118. (in Ukrainian).

Abaturov AE, Nikulina AА. Molecular-genetic concept of the formation of psychological type in children with obesity associated with lactose intolerance. Zdorov'ye Rebenka. 2017;12(4):435-440. doi: 10.22141/2224-0551.12.4.2017.1076222. (in Ukrainian).

International Association for the Study of Obesity. Online database of national prevalence data from published national surveys. London: IASO; 2014.

Kiess W, Penke M, Sergeyev E, et al. Childhood obesity at the crossroads. J Pediatr Endocrinol Metab. 2015 May;28(5-6):481-4. doi: 10.1515/jpem-2015-0168.

Lissner L, Lanfer A, Gwozdz W, et al. Television habits in relation to overweight, diet and taste preferences in European children: the IDEFICS study. Eur J Epidemiol. 2012 Sep;27(9):705-15. doi: 10.1007/s10654-012-9718-2.

Martin RM, Patel R, Zinovik A, et al. Filter paper blood spot enzyme linked immunoassay for insulin and application in the evaluation of determinants of child insulin resistance. PLoS One. 2013 Aug 1;8(8):e71315. doi: 10.1371/journal.pone.0071315. Print 2013.

McCarthy HD, Cole TJ, Fry T, Jebb SA, Prentice AM. Body fat reference curves for children. Int J Obes (Lond). 2006 Apr;30(4):598-602. doi: 10.1038/sj.ijo.0803232.

Paasela M, Kolho K-L, Vaarala O, Honkanen J. Lactose inhibits regulatory T-cell-mediated suppression of effector T-cell interferon-γ and IL-17 production. Br J Nutr. 2014 Dec 14;112(11):1819-25. doi:10.1017/S0007114514001998.

Peplies J, Börnhorst C, Günther K, et al. Longitudinal associations of lifestyle factors and weight status with insulin resistance (HOMA-IR) in preadolescent children: the large prospective cohort study IDEFICS. Int J Behav Nutr Phys Act. 2016 Sep 2;13(1):97. doi: 10.1186/s12966-016-0424-4.

Qiu X, Dao H, Wang M, et al. Insulin and Leptin Signaling Interact in the Mouse Kiss1 Neuron during the Peripubertal Period. PLoS One. 2015;10(5):e0121974. doi: 10.1371/journal.pone.0121974.

Reinehr T. Metabolic Syndrome in Children and Adolescents: a Critical Approach Considering the Interaction between Pubertal Stage and Insulin Resistance. Curr Diab Rep. 2016 Jan;16(1):8. doi: 10.1007/s11892-015-0695-1.

Reinehr T, Wolters B, Knop C, Lass N, Holl RW. Strong effect of pubertal status on metabolic health in obese children: a longitudinal study. J Clin Endocrinol Metab. 2015 Jan;100(1):301-8. doi: 10.1210/jc. 2014-2674.

Schwandt P, von Eckardstein A, Haas GM. Percentiles of Percentage Body Fat in German Children and Adolescents: An International Comparison. Int J Prev Med. 2012 Dec;3(12):846-852. PMID: 23272283.

WHO European Childhood Obesity Surveillance Initiative (COSI). Available from: http://www.euro.who.int/en/health-topics/disease-prevention/nutrition/activities/who-european-childhood-obesity-surveillance-initiative-cosi. Accessed June 24, 2014.

Wijnhoven TM, van Raaij JM, Spinelli A, et al. WHO European Childhood Obesity Surveillance Initiative 2008: weight, height and body mass index in 6-9-year-old children. Pediatr Obes. 2013 Apr;8(2):79-97. doi: 10.1111/j.2047-6310.2012.00090.x.




DOI: https://doi.org/10.22141/2224-0551.12.8.2017.119243

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