The Cooperation among Insulin, Cortisol and Thyroid Hormones in Morbid Obese Children and Metabolic Syndrome
Authors: Orkide Donma, Mustafa M. Donma
Abstract:
Obesity, a disease associated with a low-grade inflammation, is a risk factor for the development of metabolic syndrome (MetS). So far, MetS risk factors such as parameters related to glucose and lipid metabolisms as well as blood pressure were considered for the evaluation of this disease. There are still some ambiguities related to the characteristic features of MetS observed particularly in pediatric population. Hormonal imbalance is also important, and quite a lot information exists about the behaviour of some hormones in adults. However, the hormonal profiles in pediatric metabolism have not been cleared yet. The aim of this study is to investigate the profiles of cortisol, insulin, and thyroid hormones in children with MetS. The study population was composed of morbid obese (MO) children without (Group 1) and with (Group 2) MetS components. WHO BMI-for age and sex percentiles were used for the classification of obesity. The values above 99 percentile were defined as morbid obesity. Components of MetS (central obesity, glucose intolerance, high blood pressure, high triacylglycerol levels, low levels of high density lipoprotein cholesterol) were determined. Anthropometric measurements were performed. Ratios as well as obesity indices were calculated. Insulin, cortisol, thyroid stimulating hormone (TSH), free T3 and free T4 analyses were performed by electrochemiluminescence immunoassay. Data were evaluated by statistical package for social sciences program. p<0.05 was accepted as the degree for statistical significance. The mean ages±SD values of Group 1 and Group 2 were 9.9±3.1 years and 10.8±3.2 years, respectively. Body mass index (BMI) values were calculated as 27.4±5.9 kg/m2 and 30.6±8.1 kg/m2, successively. There were no statistically significant differences between the ages and BMI values of the groups. Insulin levels were statistically significantly increased in MetS in comparison with the levels measured in MO children. There was not any difference between MO children and those with MetS in terms of cortisol, T3, T4 and TSH. However, T4 levels were positively correlated with cortisol and negatively correlated with insulin. None of these correlations were observed in MO children. Cortisol levels in both MO as well as MetS group were significantly correlated. Cortisol, insulin, and thyroid hormones are essential for life. Cortisol, called the control system for hormones, orchestrates the performance of other key hormones. It seems to establish a connection between hormone imbalance and inflammation. During an inflammatory state, more cortisol is produced to fight inflammation. High cortisol levels prevent the conversion of the inactive form of the thyroid hormone T4 into active form T3. Insulin is reduced due to low thyroid hormone. T3, which is essential for blood sugar control- requires cortisol levels within the normal range. Positive association of T4 with cortisol and negative association of it with insulin are the indicators of such a delicate balance among these hormones also in children with MetS.
Keywords: Children, cortisol, insulin, metabolic syndrome, thyroid hormones.
Digital Object Identifier (DOI): doi.org/10.5281/zenodo.1316646
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[1] P. Wolf, Y. Winhofer, M. Krššák, M. Krebs, “Heart, lipids and hormones,” Endocr Connect, vol. 6, no. 4, pp. R59-R69, May 2017.
[2] CG Magnussen, J Koskinen, W Chen, R Thomson, M. D. Schmidt, S. R. Srinivasan, M. Kivimäki, N. Mattsson, M. Kähönen, T. Laitinen, L. Taittonen, T. Rönnemaa, J. S. Viikari, G. S. Berenson, M. Juonala, and O. T. Raitakari, “Pediatric metabolic syndrome predicts adulthood metabolic syndrome, subclinical atherosclerosis, and type 2 diabetes mellitus but is no better than body mass index alone: the Bogalusa Heart Study and the Cardiovascular Risk in Young Finns Study,” Circulation, vol. 122, no.16,pp. 1604-1611, Oct. 2010.
[3] J. C. Lopez-Alvarenga, L. García-Hidalgo, M. V. Landa-Anell, R. Santos-Gómez, J. González-Barranco, and A. Comuzzie, “Influence of skin color on the diagnostic utility of clinical acanthosis nigricans to predict insulin resistance in obese patients,” Arch Med Res, vol. 37, no. 6, pp.744-748, Aug. 2006.
[4] C. Langrock, J. Heebrand, K. Radowski, E. Hamelmann, T. Lücke, M. Holtmann, T. Legenbauer, B. Schmidt, M. Frank, K. H. Jöckel, and T. Reinehr T, “Thyroid Hormone Status in Overweight Children with Attention Deficit/Hyperactivity Disorder,” Horm Res Paediatr, Jan. 2018 (Epub ahead of print).
[5] E. Ozcelik, S. Uslu, N. Kebapçı, M. Kara M, A. Dokumacıoğlu, and A. Musmul, “Interrelations of serum leptin levels with adrenocorticotropic hormone, basal cortisol and dehydroepiandrosterone sulphate levels in patients with metabolic syndrome” Diabetes Met Syndr Clin Res Rev, vol. 4, no. 1, pp. 13-17, Jan.-Mar. 2010.
[6] World Health Organization (WHO). The WHO Child Growth Standarts. Available at: http:// www.who.int /childgrowth/en/. Accessed on June 10, 2016.
[7] P. Zimmet, K. G. Alberti, F. Kaufman, N. Tajima, M. Silink, S. Arslanian, G. Wong, P. Bennett, J. Shaw, S. Caprio, and IDF consensus group, “The metabolic syndrome in children and adolescents-an IDF consensus report”, Pediatr. Diabetes, vol: 8, no.5, pp. 299-306, Oct. 2007.
[8] E. Atlantis, “Obesity and increased risk of type 2 diabetes mellitus: The aetiological role of depression,” Obes Res Clin Pract, vol. 6, no. 3, pp. e175-262. Jul.-Sept. 2012.
[9] P. Li, F. Pan, Y. Hao, W. Feng, H. Song, and D. Zhu, “SGK1 is regulated by metabolic-related factors in 3T3-L1 adipocytes and overexpressed in the adipose tissue of subjects with obesity and diabetes,” Diabetes Res Clin Pract, vol. 102, no. 1, p.35-42, Oct. 2013.
[10] S. E. Walker, M. E. Smolkin, M. L. O'Leary, S. B. Cluett, V. F. Norwood, M. D. Deboer, and M. J. Gurka, “Predictors of retention and BMI loss or stabilization in obese youth enrolled in a weight loss intervention, Obes Res Clin Pract, vol.6, no.4, pp. e263-346, Oct.- Dec. 2012.
[11] J. A. de Souza, C. Vindis, B. Hansel, A. Nègre-Salvayre, P. Therond, C. V. Serrano, S. Chantepie, R. Salvayre, E. Bruckert, M. J. Chapman, and A. Kontush,” “Metabolic syndrome features small, apolipoprotein A-I-poor, triglyceride-rich HDL3 particles with defective anti-apoptotic activity,” Atherosclerosis, vol.197, no.1, pp. 84-94, Mar. 2008.
[12] N. Saigi-Morgui, F. Vandenberghe, A. Delacrétaz, L. Quteineh, M. Gholamrezaee, J. M. Aubry, A. von Gunten, Z. Kutalik, P. Conus, and C. B. Eap, “Association of genetic risk scores with body mass index in Swiss psychiatric cohorts,” Pharmacogenet Genomics, vol.26, no. 5, pp. 208-217, May 2016.
[13] M. J. Weigensberg, C. M. Toledo-Corral, and M. I. Goran, “Association between the metabolic syndrome and serum cortisol in overweight Latino youth,” J Clin Endocrinol Metab, vol. 93, no. 4, pp. 1372-1378, Apr. 2008.
[14] Y. Sen, D. Aygun, E. Yilmaz, and A. Ayar, “Children and adolescents with obesity and the metabolic syndrome have high circulating cortisol levels,” Neuro Endocrinol Lett, vol. 29, no. 1, pp. 141-145, Feb. 2008.
[15] B. G. Bhat, H. Younis, J. Herrera, K. Palacio, B. Pascual, G. Hur, B. Jessen, K. M. Ogilvie, and P. A. Rejto, “Antisense inhibition of 11betahydroxysteroid dehydrogenase type 1 improves diabetes in a novel cortisone-induced diabetic KK mouse model,” Biochem Biophys Res Commun, vol. 365, no. 4, pp. 740-745, Jan.2008.
[16] G. Radetti, G. Grugni, F. Lupi, N. Marazzi, S. Longhi, A. Fanolla, and A. Sartorio A, “ The relationship between hyperthyrotropinemia and metabolic and cardiovascular risk factors in a large group of overweight and obese children and adolescents,” J Endocrinol Invest, vol. 40, no. 12, pp. 1311-1319, Dec. 2017.
[17] A. Shaoba, Basu S, Mantis S, and C. Minutti, “Serum thyroid-stimulating hormone levels and body mass index percentiles in children with primary hypothyroidism on levothyroxine replacement,” J Clin Res Pediatr Endocrinol, vol. 9, no. 4, pp. 337-343, Dec. 2017.
[18] V. Lundbäck, K. Ekbom, E. Hagman, I. Dahlman, and C. Marcus, “Thyroid-stimulating hormone, degree of obesity, and metabolic risk markers in a cohort of Swedish children with obesity,” Horm Res Paediatr, vol. 88, no. 2, pp. 140-146, 2017.
[19] M. Rumińska, E. Witkowska-Sędek, A. Majcher, and B. Pyrżak, “Thyroid function in obese children and adolescents and its association with anthropometric and metabolic parameters,” Adv Exp Med Biol, vol. 912, pp. 33-41, 2016.
[20] A. J. Krause, B. Cines, E. Pogrebniak, R. Sherafat-Kazemzadeh, A.P. Demidowich, O.A. Galescu, S. M. Brady, J. C. Reynolds, V. S. Hubbard, and J. A. Yanovski, “Associations between adiposity and indicators of thyroid status in children and adolescents,” Pediatr Obes, vol. 11, no. 6, pp. 551-558, Dec. 2016.
[21] E. Garcia-Garcia, M. A. Vázquez-López, E. García-Fuentes, R. Galera-Martínez, C. Gutiérrez-Repiso, I. García-Escobar, and A. Bonillo-Perales, “Thyroid function and thyroid autoimmunity in relation to weight status and cardiovascular risk factors in children and adolescents: A population-based study,” J Clin Res Pediatr Endocrinol, vol. 8, no.2, pp. 157-162, Jun. 2016.
[22] E. J. Verspohl, and M. C. Michel, “Novel pharmacological approaches to the treatment of type 2 diabetes,” Pharm Rev, vol. 64, no. 2, pp. 188-237, Apr. 2012.
[23] A. Borai, C. Livingstone, S. Mehta, H. Zarif, F. Abdelaal, and G. Ferns, “Biological variation in fasting serum insulin-like growth factor binding protein-1 (IGFBP-1) among individuals with a varying glucose tolerance,” Clin Biochem, vol. 42, no, 12, pp.1270-1274, Aug. 2009.