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Investigation of cardiovascular risk parameters in adolescents with metabolic syndrome

Published online by Cambridge University Press:  30 June 2023

Ummugulsum Can Open the ORCID record for Ummugulsum Can [Opens in a new window] ,
Sadinaz Akdu ,
Zafer Bağcı Open the ORCID record for Zafer Bağcı [Opens in a new window]  and
Muammer Buyukinan
Ummugulsum Can*
Affiliation:
Department of Biochemistry, Konya City Hospital, Konya, Turkey
Sadinaz Akdu
Affiliation:
Department of Biochemistry, Fethiye State Hospital, Muğla, Turkey
Zafer Bağcı
Affiliation:
Department of Pediatric, Konya City Hospital, Konya, Turkey
Muammer Buyukinan
Affiliation:
Department of Pediatric Endocrinology, Konya City Hospital, Konya, Turkey
*
Corresponding author: U. Can; Email: cangulsum@yahoo.com
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Abstract

Background:

Metabolic syndrome leading to type 2 diabetes mellitus and cardiovascular diseases is a chronic multifactorial syndrome, associated with low-grade inflammation status. In our study, we aimed at assessing the serum levels of follistatin (FST), pregnancy-associated plasma protein-A (PAPP-A), and platelet/endothelial cell adhesion molecule-1 (PECAM-1) in adolescent patients with metabolic syndrome.

Methods:

This study was performed in 43 (19 males, 24 females) metabolic syndrome adolescents and 37 lean controls matched for age and sex. The serum levels of FST, PECAM-1, and PAPP-A were measured by using ELISA method.

Results:

Serum FST and PAPP-A levels in metabolic syndrome were significantly higher than those of controls (p < 0.005 and p < 0.05). However, there was no difference in serum PECAM-1 levels between metabolic syndrome and control groups (p = 0.927). There was a significant positive correlation between serum FST and triglyceride (r = 0.252; p < 0.05), and PAPP-A and weight, (r = 0.252; p < 0.05) in metabolic syndrome groups. Follistatin was determined statistically significant in both univariate (p = 0,008) and multivariate (p = 0,011) logistic regression analysis.

Conclusions:

Our findings indicated a significant relationship between FST and PAPP-A levels and metabolic syndrome. These findings offer the possibility of using these markers in diagnosis of metabolic syndrome in adolescents as the prevention of the future complications.

Keywords

Metabolic syndromefollistatinpregnancy-associated plasma protein-Aplatelet/endothelial cell adhesion molecule-1
Type
Original Article
Information
Cardiology in the Young , Volume 34 , Issue 2 , February 2024 , pp. 308 - 313
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Copyright
© The Author(s), 2023. Published by Cambridge University Press

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References

Can, U, Buyukinan, M, Guzelant, A, et al. Investigation of the inflammatory biomarkers of metabolic syndrome in adolescents. J Pediatr Endocrinol Metab 2016; 29: 1277–1283.Google ScholarPubMed
Ennequin, G, Sirvent, P, Whitham, M. Role of exercise-induced hepatokines in metabolic disorders. Am J Physiol Endocrinol Metab 2019; 317: E11–E24.CrossRefGoogle ScholarPubMed
Silva, RN, Bueno, PG, Avó, LR, et al. Effect of physical training on liver expression of activin a and follistatin in a nonalcoholic fatty liver disease model in rats. Braz J Med Biol Res 2014; 47: 746–752.CrossRefGoogle Scholar
Singh, R, Braga, M, Pervin, S. Regulation of brown adipocyte metabolism by myostatin/follistatin signaling. Front Cell Dev Biol 2014; 2: 60.CrossRefGoogle ScholarPubMed
Li, H, Zhang, C, Liu, J, et al. Intraperitoneal administration of follistatin promotes adipocyte browning in high-fat diet-induced obese mice. PLoS One 2019; 14: e0220310.CrossRefGoogle ScholarPubMed
Conover, CA, Harstad, SL, Tchkonia, T, et al. Preferential impact of pregnancy-associated plasma protein-a deficiency on visceral fat in mice on high-fat diet. Am J Physiol Endocrinol Metab 2013; 305: E1145–1153.CrossRefGoogle ScholarPubMed
Sangiorgi, G, Mauriello, A, Bonanno, E, et al. Pregnancy-associated plasma protein-a is markedly expressed by monocyte-macrophage cells in vulnerable and ruptured carotid atherosclerotic plaques: a link between inflammation and cerebrovascular events. J Am Coll Cardiol 2006; 47: 2201e11.CrossRefGoogle ScholarPubMed
Li, WP, Neradilek, MB, Gu, FS, et al. Pregnancy-associated plasma protein-a is a stronger predictor for adverse cardiovascular outcomes after acute coronary syndrome in type-2 diabetes mellitus. Cardiovasc Diabetol 2017; 16: 45.CrossRefGoogle ScholarPubMed
Serebruany, VL, Gurbel, PA. Effect of thrombolytic therapy on platelet expression and plasma concentration of PECAM-1 (CD31) in patients with acute myocardial infarction. Arterioscler Thromb Vasc Biol 1999; 19: 153–158.CrossRefGoogle ScholarPubMed
Sun, QH, DeLisser, HM, Zukowski, MM, et al. Individually distinct Ig homology domains in PECAM-1 regulate homophilic binding and modulate receptor affinity. J Biol Chem 1996; 271: 11090–11098.CrossRefGoogle ScholarPubMed
Kjaergaard, AG, Dige, A, Krog, J, et al. Soluble adhesion molecules correlate with surface expression in an in vitro model of endothelial activation. Basic Clin Pharmacol Toxicol 2013; 113: 273–279.CrossRefGoogle Scholar
Neyzi, O, Furman, A, Bundak, R, et al. Growth references for turkish children aged 6 to 18 years. Acta Paediatr 2006; 95: 1635–1641.CrossRefGoogle ScholarPubMed
Bundak, R, Furman, A, Gunoz, H, et al. Body mass index references for turkish children. Acta Paediatr 2006; 9: 194–198.CrossRefGoogle Scholar
Zimmet, P, Alberti, KG, Kaufman, F, et al. The metabolic syndrome in children and adolescents- an IDF consensus report. Pediatr Diabetes 2007; 8: 299–306.CrossRefGoogle ScholarPubMed
Marshall, WA, Tanner, JM. Variations in the pattern of pubertal changes in boys. Arch Dis Child 1970; 45: 13–4523.CrossRefGoogle ScholarPubMed
Hatipoglu, N, Ozturk, A, Mazicioglu, MM, et al. Waist circumference percentiles for 7-17 year old turkish children and adolescents. Eur J Pediatr 2008; 167: 383–389.CrossRefGoogle ScholarPubMed
National High Blood Pressure Education Program Working Group on High Blood Pressure in Children and Adolescents. The fourth report on the diagnosis, evaluation, and treatment of high blood pressure in children and adolescents. Pediatrics 2004; 114: 555–576.CrossRefGoogle Scholar
Keskin, M, Kurtoglu, S, Kendirci, M, et al. Homeostasis model assessment is more reliable than the fasting glucose/insulin ratio and quantitative insulin sensitivity check index for assessing insulin resistance among obese children and adolescents. Pediatrics 2005; 115: e500–e503.CrossRefGoogle Scholar
Eckel, RH, Grundy, SM, Zimmet, PZ. The metabolic syndrome. Lancet 2005; 365: 1415–1428.CrossRefGoogle ScholarPubMed
Perakakis, N, Kokkinos, A, Peradze, N, et al. Follistatins in glucose regulation in healthy and obese individuals. Diabetes Obes Metab 2019; 21: 683–690.CrossRefGoogle ScholarPubMed
Davey, JR, Estevez, E, Thomson, RE, et al. Intravascular follistatin gene delivery improves glycemic control in a mouse model of type 2 diabetes. FASEB J 2020; 34: 5697–5714.CrossRefGoogle Scholar
Perakakis, N, Mougios, V, Fatouros, I, et al. Physiology of activins/follistatins:associations with metabolic and anthropometric variables and response to exercise. J Clin Endocrinol Metab 2018; 103: 3890–3899.CrossRefGoogle ScholarPubMed
Singh, R, Pervin, S, Lee, SJ, et al. Metabolic profiling of follistatin overexpression: a novel therapeutic strategy for metabolic diseases. Diabetes Metab Syndr Obes 2018; 11: 65–84.CrossRefGoogle ScholarPubMed
Tang, R, Harasymowicz, NS, Wu, CL, et al. Gene therapy for follistatin mitigates systemic metabolic inflammation and post-traumatic arthritis in high-fat diet-induced obesity. Sci Adv 2020; 6: eaaz7492.CrossRefGoogle ScholarPubMed
Tao, R, Wang, C, Stöhr, O, et al. Inactivating hepatic follistatin alleviates hyperglycemia. Nat Med 2018; 24: 1058–1069.CrossRefGoogle ScholarPubMed
Frias Fde, T, de Mendonça, M, Martins, AR, et al. Myomirs as markers of insulin resistance and decreased myogenesis in skeletal muscle of diet-induced obese mice. Front Endocrinol (Lausanne) 2016; 7: 76.Google ScholarPubMed
Woelfle, J, Roth, CL, Wunsch, R, Reinehr, T. Pregnancy-associated plasma protein a in obese children relationship to markers and risk factors of atherosclerosis and members of the IGF system. Eur J Endocrinol 2011; 165: 613–622.CrossRefGoogle ScholarPubMed
Aso, Y, Okumura, K, Wakabayashi, S, et al. Elevated pregnancy-associated plasma protein-a in sera from type 2 diabetic patients with hypercholesterolemia: associations with carotid atherosclerosis and toe-brachial index. J Clin Endocr Metab 2004; 89: 5713–5717.CrossRefGoogle ScholarPubMed
Gude, MF, Hjortebjerg, R, Oxvig, C, etal, PAPP-A. IGFBP-4 and IGF-iI are secreted by human adipose tissue cultures in a depot-specific manner. Eur J Endocrinol 2016; 175: 509–519.CrossRefGoogle Scholar
Bonaca, MP, Scirica, BM, Sabatine, MS, et al. Prospective evaluation of pregnancy-associated plasma protein-a and outcomes in patients with acute coronary syndromes. J Am Coll Cardiol 2012; 60: 332–338.CrossRefGoogle ScholarPubMed
Bayes-Genis, A, Conover, CA, Overgaard, MT, et al. Pregnancyassociated plasma protein a as a marker of acute coronary syndromes. N Engl J Med 2001; 345: 1022–1029.CrossRefGoogle Scholar
Davidge-Pitts, C, Escande, CJ, Conover, CA. Preferential expression of PAPPA in human preadipocytes from omental fat. J Endocrinol 2014; 222: 87–97.CrossRefGoogle ScholarPubMed
Hill, CM, Arum, O, Boparai, RK, et al. Female PAPP-a knockout mice are resistant to metabolic dysfunction induced by high-fat/high-sucrose feeding at middle age. Age (Dordr) 2015; 37: 9765.CrossRefGoogle ScholarPubMed
Rosenblum, WI, Nelson, GH, Wormley, B, et al. Role of platelet-endothelial cell adhesion molecule (PECAM) in platelet adhesion/aggregation over injured but not denuded endothelium in vivo and ex vivo. Stroke 1996; 27: 709–711.CrossRefGoogle Scholar
Shamseddin, A, Crauste, C, Durand, E, et al. Resveratrol-linoleate protects from exacerbated endothelial permeability via a drastic inhibition of the MMP-9 activity. Biosci Rep 2018; 38: BSR20171712.CrossRefGoogle Scholar
Ilan, N, Mohsenin, A, Cheung, L, Madri, JA. PECAM-1 shedding during apoptosis generates a membrane-anchored truncated molecule with unique signaling characteristics. FASEB J 2001; 15: 362–372.CrossRefGoogle ScholarPubMed
Ollivier, V, Arnaud, B, Jandrot-Perrus, M, Ajzenberg, N. Monocytes downregulate the early stage of collagen-induced platelet activation by a PECAM-1-dependent mechanism. J Thromb Haemost 2009; 7: 143–151.CrossRefGoogle ScholarPubMed
Wei, H, Fang, L, Song, J, Chatterjee, S. Statin-inhibited endothelial permeability could be associated with its effect on PECAM-1 in endothelial cells. FEBS Lett 2005; 579: 1272–1278.CrossRefGoogle ScholarPubMed
Nelissen, I, Ronsse, I, Van Damme, J, Opdenakker, G. Regulation of gelatinase B in human monocytic and endothelial cells by PECAM-1 ligation and its modulation by interferon-beta. J Leukoc Biol 2002; 71: 89–98.CrossRefGoogle ScholarPubMed
Soeki, T, Tamura, Y, Shinohara, H, et al. Increased soluble platelet/endothelial cell adhesion molecule-1 in the early stages of acute coronary syndromes. Int J Cardiol 2003; 90: 261–268.CrossRefGoogle ScholarPubMed