Associations among Fetuin A, Cortisol and Thyroid Hormones in Children with Morbid Obesity and Metabolic Syndrome
Obesity is a disease with an ever-increasing prevalence throughout the world. The metabolic network associated with obesity is very complicated. In metabolic syndrome (MetS), it becomes even more difficult to understand. Within this context, hormones, cytokines, and many others participate in this complex matrix. The collaboration among all of these parameters is a matter of great wonder. Cortisol, as a stress hormone, is closely associated with obesity. Thyroid hormones are involved in the regulation of energy as well as glucose metabolism with all of its associates. Fetuin A has been known for years; however, the involvement of this parameter in obesity discussions is rather new. Recently, it has been defined as one of the new generation markers of obesity. In this study, the aim was to introduce complex interactions among all to be able to make clear comparisons, at least for a part of this complicated matter. Morbid obese (MO) children participated in the study. Two groups with 46 MO children and 43 with MetS were constituted. All children included in the study were above 99th age- and sex-adjusted body mass index (BMI) percentiles according to World Health Organization criteria. Forty-three morbid obese children in the second group also had MetS components. Informed consent forms were filled by the parents of the participants. The institutional ethics committee has given approval for the study protocol. Data as well as the findings of the study were evaluated from a statistical point of view. Two groups were matched for their age and gender compositions. Significantly higher body mass index (BMI), waist circumference, thyrotropin, and insulin values were observed in the MetS group. Triiodothyronine concentrations did not differ between the groups. Elevated levels for thyroxin, cortisol, and fetuin-A were detected in the MetS group compared to the first group (p > 0.05). In MO MetS- group, cortisol was correlated with thyroxin and fetuin-A (p < 0.05). In the MO MetS+ group, none of these correlations were present. Instead, a correlation between cortisol and thyrotropin was found (p < 0.05). In conclusion, findings have shown that cortisol was the key player in severely obese children. The association of this hormone with the participants of thyroid hormone metabolism was quite important. The lack of association with fetuin A in the morbid obese MetS+ group has suggested the possible interference of MetS components in the behavior of this new generation obesity marker. The most remarkable finding of the study was the unique correlation between cortisol and thyrotropin in the morbid obese MetS+ group, suggesting that thyrotropin may serve as a target along with cortisol in the morbid obese MetS+ group. This association may deserve specific attention during the development of remedies against MetS in the pediatric population.
[1] S. R. Daniels, “The consequences of childhood overweight and obesity,” Future Child., vol. 16, pp. 47-67, 2006.
[2] R. Weiss, J. Dziura, T. S. Burgert, W. V. Tamborlane, S. E. Taksali, C. W. Yeckel, K. Allen, M. Lopes, M. Savoye, J. Morrison, R. S. Sherwin, and S. Caprio, “Obesity and the metabolic syndrome in children and adolescents,” N. Engl. J. Med., vol. 350, pp. 2362-2374, 2004.
[3] A. M. Cali, and S. Caprio, “Obesity in children and adolescents,” J. Clin. Endocrinol. Metab., vol. 93, pp. 31-36, 2008.
[4] S. R. Ammar, T. A. Elbedewy H. M. Nagy, and N. A. Kotb, “Relationship between serum fetuin A and insulin resistance in patients with hyperthyroidism,” Tanta Med. J., vol.45, pp. 135-140, 2017
[5] E. R. Smith, R. Nilforooshan, G. Weaving, and N. Tabet, “Plasma fetuin-A is associated with the severity of cognitive impairment in mild-to-moderate Alzheimer's disease,” J. Alzheimers Dis., vol. 24, no. 2, pp. 327-333, 2011.
[6] S. Liu, W. Hu, Y. He, L. Li, H. Liu, L. Gao, G. Yang, and X. Liao, “Serum Fetuin-A levels are increased and associated with insulin resistance in women with polycystic ovary syndrome,” BMC Endocr. Disord., vol. 20, no. 1, pp. 67, May 2020.
[7] L. Bourebaba, and K. Marycz, “Pathophysiological implication of fetuin-A glycoprotein in the development of metabolic disorders: A concise review,” J. Clin. Med., vol. 8, no. 12, pp. 2033, Nov. 2019.
[8] O. Bakiner, E. Bozkirli, D. Ertugrul, N. Sezgin, and E. Ertorer, “Plasma fetuin-A levels are reduced in patients with hypothyroidism,” Eur. J. Endocrinol., vol. 170, no. 3, pp. 411-418, Feb. 2014.
[9] B. O. Pamuk, H. Yilmaz, T. Topcuoglu, O. Bilgir, O. Çalan, G. Pamuk, and D. T. Ertugrul, “Fetuin-A levels in hyperthyroidism,” Clinics (Sao Paulo)., vol. 68, no. 3, pp. 379-383, 2013.
[10] F-Y. Tseng, Y. T. Chen, Y. C. Chi, P. L. Chen, and W. S. Yang, “Serum levels of fetuin-A are negatively associated with log transformation levels of thyroid-stimulating hormone in patients with hyperthyroidism or euthyroidism: An observational study at a medical center in Taiwan,” Medicine (Baltimore)., vol. 97, no. 46, pp. e13254, Nov. 2018.
[11] X. R. Deng, L. Ding, T. G. Wang, M. Xu, J. L. Lu, M. Li, Z. Y. Zhao, Y. H. Chen, Y. F. Bi, Y. P. Xu, and Y. Xu, “Serum fetuin-A levels and thyroid function in middle-aged and elderly Chinese,” Biomed. Environ. Sci., vol. 30, no. 6, pp. 455-459, Jun. 2017.
[12] S. H. Kim, S. E. Kim, M. H. Choi, and M. J. Park, “Altered glucocorticoid metabolism in girls with central obesity,” Mol. Cell. Endocrinol., no. 111225, Feb. 2021.
[13] B. Kluwe, S. Zhao, D. Kline, R. Ortiz, G. Brock, J. B. Echouffo-Tcheugui, M. Sims, R. R. Kalyani, S. H. Golden, and J. J. Joseph, “Adiposity measures and morning serum cortisol in African Americans: Jackson Heart Study,” Obesity (Silver Spring)., vol. 29, no. 2, pp. 418-427, Feb. 2021.
[14] A. J. Anderson, R. Andrew, N. Z. M. Homer, K. A. Hughes, L. D. Boyle, M. Nixon, F. Karpe, R. H. Stimson, and B. R. Walker, “Effects of obesity and insulin on tissue-specific recycling between cortisol and cortisone in men,” J. Clin. Endocrinol. Metab., no. dgaa896, Dec. 2020.
[15] K. H. Ladwig, S. C. Schriever, S. Atasoy, M. Bidlingmaier, J. Kruse, and H. Johar, “Association of generalized and central obesity with serum and salivary cortisol secretion patterns in the elderly: findings from the cross sectional KORA-Age study,” Sci. Rep., vol. 10, no. 1 pp. 14321, Aug. 2020.
[16] I-K. Jeong, “The role of cortisol in the pathogenesis of the metabolic syndrome,” Diabetes Metab. J., vol. 36, no. 3, pp. 207–210, 2012.
[17] K. Tyagi, N. B. Agarwal, P. Kapur, S. Kohli, and R. K. Jalali, “Evaluation of stress and associated biochemical changes in patients with Type 2 diabetes mellitus and obesity,” Diabetes Metab. Syndr. Obes., vol. 14, pp. 705-717, Feb. 2021.
[18] K. N. Walter, E. J. Corwin, J. Ulbrecht, L. M. Demers, J.M. Bennett, C. A. Whetzel, and L. C. Klein, “Elevated thyroid stimulating hormone is associated with elevated cortisol in healthy young men and women,” Thyroid Res., vol. 5, no. 1, pp. 13, Oct. 2012.
[19] J. E. Silva, “The thermogenic effect of thyroid hormone and its clinical implications,” Ann. Intern. Med., vol. 139, pp. 205–213, 2003.
[20] N. Knudsen, P. Laurberg, L. B. Rasmussen, I. Bülow, H. Perrild, L. Ovesen, and T. Jørgensen. “Small differences in thyroid function may be important for body mass index and the occurrence of obesity in the population,” J. Clin. Endocrinol. Metab., vol. 90, no. 7, pp. 4019-4024, Jul. 2005.
[21] E. Maratou, D. J. Hadjidakis, M. Peppa, M. Alevizaki, K. Tsegka, V. Lambadiari, P. Mitrou, E. Boutati, A. Kollias, T. Economopoulos, S. A. Raptis, and G. Dimitriadis, “Studies of insulin resistance in patients with clinical and subclinical hyperthyroidism,” Eur. J. Endocrinol., vol. 163, no.4, pp. 625-630, Oct. 2010.
[22] S. Danzi, and I. Klein, “Thyroid hormone and the cardiovascular system,” Med. Clin. North Am., vol. 96, pp. 257–268, 2012.
[23] N. Pontikides, and G. E. Krassas, “Basic endocrine products of adipose tissue in states of thyroid dysfunction,” Thyroid, vol. 17, pp. 421–431, 2007.
[24] World Health Organization (WHO). The WHO Child Growth Standards. Available at: http://www.who.int/childgrowth/en/ Accessed on June 10, 2016.
[25] 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.
[26] X. Pan, S. W. Wen, P.L. Bestman, A. C. Kaminga, K. Acheampong, and A. Liu, “Fetuin-A in metabolic syndrome: A systematic review and meta-analysis,” PLoS One., vol. 15, no. 3, pp. e0229776, Mar. 2020.
[27] V. Kasabri, S. Shawakri, A. Akour, R. Naffa, N. Khawaja, I. Al-Sarraf, and J. Bzour, “Cross-sectional correlates of increased IL-18 but reduced fetuin-A and oxytocin with adiposity and blood indices in metabolic syndrome patients with and without prediabetes,” Ther. Adv. Endocrinol. Metab., vol. 9, no. 12, pp. 329–338, Aug. 2018.
[28] I. Jialal, S. Devaraj, A. Bettaieb, F. Haj, and B. Adams-Huet, “Increased adipose tissue secretion of Fetuin-A, lipopolysaccharide-binding protein and high-mobility group box protein 1 in metabolic syndrome,” Atherosclerosis, vol. 241, no.1, pp. 130–137, 2015.
[29] Z. W. Zhou, H. X. Ju, M. Z. Sun, H. M. Chen, Q. P. Fu, and D. M. Jiang, “Serum fetuin-A levels in obese and non-obese subjects with and without type 2 diabetes mellitus,” Clin. Chim. Acta., vol. 476, pp. 98-102, Jan. 2018.
[30] P. F. D. S.Teixeira, P. B. Dos Santos, and C. C. Pazos-Moura, “The role of thyroid hormone in metabolism and metabolic syndrome,” Ther. Adv. Endocrinol. Metab., vol. 11, no. 2042018820917869, May 2020.
[31] H. T. Park, G. J. Cho, K. H. Ahn, J. H. Shin, S. C. Hong, T. Kim, J. Y. Hur, Y. T. Kim, K. W. Lee, and S. H. Kim, “Thyroid stimulating hormone is associated with metabolic syndrome in euthyroid postmenopausal women,” Maturitas., vol.62, no. 3, pp. 301-305, Mar. 2009.
[32] S. Ruhla, M. O. Weickert, A. M. Arafat, M. Osterhoff, F. Isken, J. Spranger, C. Schöfl, A. F. Pfeiffer, and M. Möhlig, “A high normal TSH is associated with the metabolic syndrome,” Clin Endocrinol (Oxf)., vol. 2, no. 5, pp. 696-701, May 2010.
[33] Y. Lai, J. Wang, F. Jiang, B. Wang, Y. Chen, M. Li, H. Liu, C. Li, H. Xue, N. Li, J. Yu, L. Shi, X. Bai, X. Hou, L. Zhu, L. Lu, S. Wang, Q. Xing, X. Teng, W. Teng, and Z. Shan, “The relationship between serum thyrotropin and components of metabolic syndrome,” Endocr J., vol. 58, no.1 pp. 23-30, 2011.
[34] L. Kannan, S. Pomerantz, and A. Chernoff, “Hypothyroidism and the metabolic syndrome,” Endocrinol. Metab. Int. J., vol. 5, no. 2, pp. 188-191, 2017.
[35] S. Longhi, and G. Radetti, “Thyroid function and obesity, J. Clin. Res. Pediatr. Endocrinol., vol.5, no. Suppl 1, pp. 40-44, 2013.
[36] R. Ashley, "Elevated TSH and obesity: Cause or consequence?," Nursing Capstones, vol. 139, 2019. https://commons.und.edu/nurs-capstones/139
[37] S. Paredes, and L. Ribeiro, “Cortisol: the villain in metabolic syndrome?,” Rev. Assoc. Med. Bras., vol. 60, no. 1, pp.84-92, Jan-Feb. 2014.
[38] S. B. Abraham, D. Rubino, N. Sinaii, S. Ramsey, and L. K. Nieman, “Cortisol, obesity, and the metabolic syndrome: a cross-sectional study of obese subjects and review of the literature,” Obesity (Silver Spring)., vol. 21, no. 1, pp. E105-17, Jan. 2013.
[39] P. Anagnostis, V. G. Athyros, K. Tziomalos, A. Karagiannis, and D. P. Mikhailidis, “The pathogenetic role of cortisol in the metabolic syndrome: A hypothesis,” J. Clin. Endocrinol. Metab., vol. 94, no. 8, pp. 2692–2701, Aug. 2009.
[40] P. Constantinopoulos, M. Michalaki, A. Kottorou, I. Habeos, A. Psyrogiannis, F. F. Kalfarentzos, and V. Kyriazopoulou, “Cortisol in tissue and systemic level as a contributing factor to the development of metabolic syndrome in severely obese patients,” Eur. J. Endocrinol.,vol.172, no. 1, pp. 69-78, 2015.
[41] A. Sorisky, T. T. Antunes, and A. Gagnon, “The adipocyte as a novel TSH target,” Mini Rev. Med. Chem., vol. 8, no. 1, pp. 91-96, Jan. 2008
[1] S. R. Daniels, “The consequences of childhood overweight and obesity,” Future Child., vol. 16, pp. 47-67, 2006.
[2] R. Weiss, J. Dziura, T. S. Burgert, W. V. Tamborlane, S. E. Taksali, C. W. Yeckel, K. Allen, M. Lopes, M. Savoye, J. Morrison, R. S. Sherwin, and S. Caprio, “Obesity and the metabolic syndrome in children and adolescents,” N. Engl. J. Med., vol. 350, pp. 2362-2374, 2004.
[3] A. M. Cali, and S. Caprio, “Obesity in children and adolescents,” J. Clin. Endocrinol. Metab., vol. 93, pp. 31-36, 2008.
[4] S. R. Ammar, T. A. Elbedewy H. M. Nagy, and N. A. Kotb, “Relationship between serum fetuin A and insulin resistance in patients with hyperthyroidism,” Tanta Med. J., vol.45, pp. 135-140, 2017
[5] E. R. Smith, R. Nilforooshan, G. Weaving, and N. Tabet, “Plasma fetuin-A is associated with the severity of cognitive impairment in mild-to-moderate Alzheimer's disease,” J. Alzheimers Dis., vol. 24, no. 2, pp. 327-333, 2011.
[6] S. Liu, W. Hu, Y. He, L. Li, H. Liu, L. Gao, G. Yang, and X. Liao, “Serum Fetuin-A levels are increased and associated with insulin resistance in women with polycystic ovary syndrome,” BMC Endocr. Disord., vol. 20, no. 1, pp. 67, May 2020.
[7] L. Bourebaba, and K. Marycz, “Pathophysiological implication of fetuin-A glycoprotein in the development of metabolic disorders: A concise review,” J. Clin. Med., vol. 8, no. 12, pp. 2033, Nov. 2019.
[8] O. Bakiner, E. Bozkirli, D. Ertugrul, N. Sezgin, and E. Ertorer, “Plasma fetuin-A levels are reduced in patients with hypothyroidism,” Eur. J. Endocrinol., vol. 170, no. 3, pp. 411-418, Feb. 2014.
[9] B. O. Pamuk, H. Yilmaz, T. Topcuoglu, O. Bilgir, O. Çalan, G. Pamuk, and D. T. Ertugrul, “Fetuin-A levels in hyperthyroidism,” Clinics (Sao Paulo)., vol. 68, no. 3, pp. 379-383, 2013.
[10] F-Y. Tseng, Y. T. Chen, Y. C. Chi, P. L. Chen, and W. S. Yang, “Serum levels of fetuin-A are negatively associated with log transformation levels of thyroid-stimulating hormone in patients with hyperthyroidism or euthyroidism: An observational study at a medical center in Taiwan,” Medicine (Baltimore)., vol. 97, no. 46, pp. e13254, Nov. 2018.
[11] X. R. Deng, L. Ding, T. G. Wang, M. Xu, J. L. Lu, M. Li, Z. Y. Zhao, Y. H. Chen, Y. F. Bi, Y. P. Xu, and Y. Xu, “Serum fetuin-A levels and thyroid function in middle-aged and elderly Chinese,” Biomed. Environ. Sci., vol. 30, no. 6, pp. 455-459, Jun. 2017.
[12] S. H. Kim, S. E. Kim, M. H. Choi, and M. J. Park, “Altered glucocorticoid metabolism in girls with central obesity,” Mol. Cell. Endocrinol., no. 111225, Feb. 2021.
[13] B. Kluwe, S. Zhao, D. Kline, R. Ortiz, G. Brock, J. B. Echouffo-Tcheugui, M. Sims, R. R. Kalyani, S. H. Golden, and J. J. Joseph, “Adiposity measures and morning serum cortisol in African Americans: Jackson Heart Study,” Obesity (Silver Spring)., vol. 29, no. 2, pp. 418-427, Feb. 2021.
[14] A. J. Anderson, R. Andrew, N. Z. M. Homer, K. A. Hughes, L. D. Boyle, M. Nixon, F. Karpe, R. H. Stimson, and B. R. Walker, “Effects of obesity and insulin on tissue-specific recycling between cortisol and cortisone in men,” J. Clin. Endocrinol. Metab., no. dgaa896, Dec. 2020.
[15] K. H. Ladwig, S. C. Schriever, S. Atasoy, M. Bidlingmaier, J. Kruse, and H. Johar, “Association of generalized and central obesity with serum and salivary cortisol secretion patterns in the elderly: findings from the cross sectional KORA-Age study,” Sci. Rep., vol. 10, no. 1 pp. 14321, Aug. 2020.
[16] I-K. Jeong, “The role of cortisol in the pathogenesis of the metabolic syndrome,” Diabetes Metab. J., vol. 36, no. 3, pp. 207–210, 2012.
[17] K. Tyagi, N. B. Agarwal, P. Kapur, S. Kohli, and R. K. Jalali, “Evaluation of stress and associated biochemical changes in patients with Type 2 diabetes mellitus and obesity,” Diabetes Metab. Syndr. Obes., vol. 14, pp. 705-717, Feb. 2021.
[18] K. N. Walter, E. J. Corwin, J. Ulbrecht, L. M. Demers, J.M. Bennett, C. A. Whetzel, and L. C. Klein, “Elevated thyroid stimulating hormone is associated with elevated cortisol in healthy young men and women,” Thyroid Res., vol. 5, no. 1, pp. 13, Oct. 2012.
[19] J. E. Silva, “The thermogenic effect of thyroid hormone and its clinical implications,” Ann. Intern. Med., vol. 139, pp. 205–213, 2003.
[20] N. Knudsen, P. Laurberg, L. B. Rasmussen, I. Bülow, H. Perrild, L. Ovesen, and T. Jørgensen. “Small differences in thyroid function may be important for body mass index and the occurrence of obesity in the population,” J. Clin. Endocrinol. Metab., vol. 90, no. 7, pp. 4019-4024, Jul. 2005.
[21] E. Maratou, D. J. Hadjidakis, M. Peppa, M. Alevizaki, K. Tsegka, V. Lambadiari, P. Mitrou, E. Boutati, A. Kollias, T. Economopoulos, S. A. Raptis, and G. Dimitriadis, “Studies of insulin resistance in patients with clinical and subclinical hyperthyroidism,” Eur. J. Endocrinol., vol. 163, no.4, pp. 625-630, Oct. 2010.
[22] S. Danzi, and I. Klein, “Thyroid hormone and the cardiovascular system,” Med. Clin. North Am., vol. 96, pp. 257–268, 2012.
[23] N. Pontikides, and G. E. Krassas, “Basic endocrine products of adipose tissue in states of thyroid dysfunction,” Thyroid, vol. 17, pp. 421–431, 2007.
[24] World Health Organization (WHO). The WHO Child Growth Standards. Available at: http://www.who.int/childgrowth/en/ Accessed on June 10, 2016.
[25] 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.
[26] X. Pan, S. W. Wen, P.L. Bestman, A. C. Kaminga, K. Acheampong, and A. Liu, “Fetuin-A in metabolic syndrome: A systematic review and meta-analysis,” PLoS One., vol. 15, no. 3, pp. e0229776, Mar. 2020.
[27] V. Kasabri, S. Shawakri, A. Akour, R. Naffa, N. Khawaja, I. Al-Sarraf, and J. Bzour, “Cross-sectional correlates of increased IL-18 but reduced fetuin-A and oxytocin with adiposity and blood indices in metabolic syndrome patients with and without prediabetes,” Ther. Adv. Endocrinol. Metab., vol. 9, no. 12, pp. 329–338, Aug. 2018.
[28] I. Jialal, S. Devaraj, A. Bettaieb, F. Haj, and B. Adams-Huet, “Increased adipose tissue secretion of Fetuin-A, lipopolysaccharide-binding protein and high-mobility group box protein 1 in metabolic syndrome,” Atherosclerosis, vol. 241, no.1, pp. 130–137, 2015.
[29] Z. W. Zhou, H. X. Ju, M. Z. Sun, H. M. Chen, Q. P. Fu, and D. M. Jiang, “Serum fetuin-A levels in obese and non-obese subjects with and without type 2 diabetes mellitus,” Clin. Chim. Acta., vol. 476, pp. 98-102, Jan. 2018.
[30] P. F. D. S.Teixeira, P. B. Dos Santos, and C. C. Pazos-Moura, “The role of thyroid hormone in metabolism and metabolic syndrome,” Ther. Adv. Endocrinol. Metab., vol. 11, no. 2042018820917869, May 2020.
[31] H. T. Park, G. J. Cho, K. H. Ahn, J. H. Shin, S. C. Hong, T. Kim, J. Y. Hur, Y. T. Kim, K. W. Lee, and S. H. Kim, “Thyroid stimulating hormone is associated with metabolic syndrome in euthyroid postmenopausal women,” Maturitas., vol.62, no. 3, pp. 301-305, Mar. 2009.
[32] S. Ruhla, M. O. Weickert, A. M. Arafat, M. Osterhoff, F. Isken, J. Spranger, C. Schöfl, A. F. Pfeiffer, and M. Möhlig, “A high normal TSH is associated with the metabolic syndrome,” Clin Endocrinol (Oxf)., vol. 2, no. 5, pp. 696-701, May 2010.
[33] Y. Lai, J. Wang, F. Jiang, B. Wang, Y. Chen, M. Li, H. Liu, C. Li, H. Xue, N. Li, J. Yu, L. Shi, X. Bai, X. Hou, L. Zhu, L. Lu, S. Wang, Q. Xing, X. Teng, W. Teng, and Z. Shan, “The relationship between serum thyrotropin and components of metabolic syndrome,” Endocr J., vol. 58, no.1 pp. 23-30, 2011.
[34] L. Kannan, S. Pomerantz, and A. Chernoff, “Hypothyroidism and the metabolic syndrome,” Endocrinol. Metab. Int. J., vol. 5, no. 2, pp. 188-191, 2017.
[35] S. Longhi, and G. Radetti, “Thyroid function and obesity, J. Clin. Res. Pediatr. Endocrinol., vol.5, no. Suppl 1, pp. 40-44, 2013.
[36] R. Ashley, "Elevated TSH and obesity: Cause or consequence?," Nursing Capstones, vol. 139, 2019. https://commons.und.edu/nurs-capstones/139
[37] S. Paredes, and L. Ribeiro, “Cortisol: the villain in metabolic syndrome?,” Rev. Assoc. Med. Bras., vol. 60, no. 1, pp.84-92, Jan-Feb. 2014.
[38] S. B. Abraham, D. Rubino, N. Sinaii, S. Ramsey, and L. K. Nieman, “Cortisol, obesity, and the metabolic syndrome: a cross-sectional study of obese subjects and review of the literature,” Obesity (Silver Spring)., vol. 21, no. 1, pp. E105-17, Jan. 2013.
[39] P. Anagnostis, V. G. Athyros, K. Tziomalos, A. Karagiannis, and D. P. Mikhailidis, “The pathogenetic role of cortisol in the metabolic syndrome: A hypothesis,” J. Clin. Endocrinol. Metab., vol. 94, no. 8, pp. 2692–2701, Aug. 2009.
[40] P. Constantinopoulos, M. Michalaki, A. Kottorou, I. Habeos, A. Psyrogiannis, F. F. Kalfarentzos, and V. Kyriazopoulou, “Cortisol in tissue and systemic level as a contributing factor to the development of metabolic syndrome in severely obese patients,” Eur. J. Endocrinol.,vol.172, no. 1, pp. 69-78, 2015.
[41] A. Sorisky, T. T. Antunes, and A. Gagnon, “The adipocyte as a novel TSH target,” Mini Rev. Med. Chem., vol. 8, no. 1, pp. 91-96, Jan. 2008
@article{"International Journal of Medical, Medicine and Health Sciences:80519", author = "Mustafa M. Donma and Orkide Donma", title = "Associations among Fetuin A, Cortisol and Thyroid Hormones in Children with Morbid Obesity and Metabolic Syndrome", abstract = "Obesity is a disease with an ever-increasing prevalence throughout the world. The metabolic network associated with obesity is very complicated. In metabolic syndrome (MetS), it becomes even more difficult to understand. Within this context, hormones, cytokines, and many others participate in this complex matrix. The collaboration among all of these parameters is a matter of great wonder. Cortisol, as a stress hormone, is closely associated with obesity. Thyroid hormones are involved in the regulation of energy as well as glucose metabolism with all of its associates. Fetuin A has been known for years; however, the involvement of this parameter in obesity discussions is rather new. Recently, it has been defined as one of the new generation markers of obesity. In this study, the aim was to introduce complex interactions among all to be able to make clear comparisons, at least for a part of this complicated matter. Morbid obese (MO) children participated in the study. Two groups with 46 MO children and 43 with MetS were constituted. All children included in the study were above 99th age- and sex-adjusted body mass index (BMI) percentiles according to World Health Organization criteria. Forty-three morbid obese children in the second group also had MetS components. Informed consent forms were filled by the parents of the participants. The institutional ethics committee has given approval for the study protocol. Data as well as the findings of the study were evaluated from a statistical point of view. Two groups were matched for their age and gender compositions. Significantly higher body mass index (BMI), waist circumference, thyrotropin, and insulin values were observed in the MetS group. Triiodothyronine concentrations did not differ between the groups. Elevated levels for thyroxin, cortisol, and fetuin-A were detected in the MetS group compared to the first group (p > 0.05). In MO MetS- group, cortisol was correlated with thyroxin and fetuin-A (p < 0.05). In the MO MetS+ group, none of these correlations were present. Instead, a correlation between cortisol and thyrotropin was found (p < 0.05). In conclusion, findings have shown that cortisol was the key player in severely obese children. The association of this hormone with the participants of thyroid hormone metabolism was quite important. The lack of association with fetuin A in the morbid obese MetS+ group has suggested the possible interference of MetS components in the behavior of this new generation obesity marker. The most remarkable finding of the study was the unique correlation between cortisol and thyrotropin in the morbid obese MetS+ group, suggesting that thyrotropin may serve as a target along with cortisol in the morbid obese MetS+ group. This association may deserve specific attention during the development of remedies against MetS in the pediatric population.", keywords = "children, cortisol, fetuin A, morbid obesity, thyrotropin", volume = "15", number = "8", pages = "203-4", }
