IRIZIN AS A MARKER OF DIABETIC MYOPATHY IN CHILDREN WITH DIABETES TYPE 1
Keywords:myopathy, irisin, Type 1 diabetes, children
The purpose of the study: to study the amount of irizin in the blood serum of children with Type 1 diabetes considering the duration of clinical course and determine the role of irizin in diagnosing the diabetic myopathy. The study included 90 children with Type 1 diabetes (T1D) (average age 13,7±0,4 years old). Depending on the duration of the disease, 3 groups were formed: 1 group — 26 children under 1 year with T1D; group 2 — 27 children — duration of T1D from 1–5 years; group 3 — 37 children with T1D duration more than 5 years. The control group included of 25 conditionally healthy children of a representative age and gender. All children were evaluated for their muscle and fat mass and their indices, ultrasound examination of skeletal muscles, and determination of irisin levels in the blood serum by ELISA. It was established that with increasing durations of T1D there was a redistribution of the component body composition in the form of a decrease in the specific the muscle mass and an increase in the percentage of fat mass, as well as changes in the ultrasound pattern of skeletal muscles characterized by a decrease in the thickness of the muscle fibers, a infraction of the normal architecture of muscle and increased echogenicity of muscle bundles. It was established that in the first years of the disease, the decrease in muscle mass was accompanied by a decrease in the level of irisin, whereas with the prolonged course of T1D there was an increase in it, which was accompanied by loss of muscle mass and infraction of the architecture of skeletal muscles. Thus, increasing the level of irisin can be used as an additional marker for the development of diabetic myopathy.
Herbert SL, Nair KS. Clin Nutr 2010; 29: 1-11. doi:http://doi.org/10.1016/j.clnu.2009.09.001.
Dyidyishko YuV, Shepelkevich AP. Med Panorama 2015;5: 45-50.
Monaco CMF, Perry RCG, Hawke TJ. Curr Opin Neurol 2017; 30(5): 545-552. doi:http://doi.org/10.1097/wco.0000000000000479.
Bostrom P, Wu J, Jedrychowski MP, et al. Nature 2012;481: 463-468. doi: http://doi.org/10.1038/nature10777.
Kurdiova T, Balaz M, Vician M, et al. J Physiol 2014;592(5): 1091-1107. doi: http://doi.org/10.1113/jphysiol.2013.264655.
Cypess AM, Lehman S, Williams G, et al. New Engl J Med 2009; 360(15): 1509-1517. doi: http://doi.org/10.1056/NEJMoa0810780.
Ates I, Arikan MF, Erdogan K, et al. Endocrine Regulations 2017; 51(1): 1-7. doi:http://doi.org/10.1515/enr-2017-0001.
Peters AM, Snelling HLR, Glass DM, Bird NJ. Brit J Anaesthesia 2011; 106(5): 719-723. doi: http://doi.org/10.1097/01.SA.0000410700.55371.0f.
Boer P. Am J Physiol Renal Physiol 1984; 247(4): 632-636.
Janssen I, Heymsfield SB, Ross R. J Am Geriatr Soc 2002; 50: 889-896.
Deurenberg, P, Weststrate JA, Seidell JC. Brit J Nutrition 1991; 65(02): 105. doi:http://doi.org/10.1079/bjn19910073.
Akay A, Gedik A, Tutus A, et al. Int Urol Nephrol 2007; 39(3): 727-730. doi:http://doi.org/10.1007/s11255-006-9133-2.
Moreno-Navarrete JM, Rtega F, Serrano M, et al. J Clin Endocrinol Metab 2013; 98(4): 769-778. doi: http://doi.org/10.1210/jc.2012-2749.
Timmons JA, Baar K, Davidsen PK, Atherton PJ. Nature 2012: 488: E9–E10. doi: http://doi.org/10.1038/nature11364.
Huh JY, Panagiotou G, Mougios V, et al. Metabolism 2012;61(12): 1725-1738. doi: http://doi.org/10.1016/j.metabol.2012.09.002.
Liu JJ, Wong MD, Toy WC, et al. J Diabetes Complications 2013; 27: 365-369. doi: http://doi.org/10.1016/j.jdiacomp.2013.03.002.
Espes J, Carlsson L, Carlsson PO. Diabet Med 2015; 32:1172-1176. doi:http://doi.org/10.1111/dme.12731.
Tsoriev TT, Belaya ZE, Rozhinskaya LY. Osteoporoz i osteopatii 2016; 1: 28-34.
Mamo Gizaw, Pandi Anandakumar, Tolessa Debela. J Pharmacopuncture 2017; 20(4): 235-242. doi: http://doi.org/10.3831/KPI.2017.20.029.
Li M. Yang M, Zhou X, et al. J Clin Endocrinol Metab 2015; 100(4): 1485-1493. doi: http://doi.org/10.1210/jc.2014-2544.
Qiu S, Cai X, Yin H, et al. Metabolism 2016; 65(6): 825-834.