Metabolic and hypoxic disorders in diabetic nephropathy development in children with diabetes mellitus type i
DOI:
https://doi.org/10.15587/2313-8416.2015.50605Keywords:
diabetes mellitus type 1, diabetic nephropathy, metabolic disorders, hypoxiaAbstract
Introduction: Diabetic nephropathy is the main cause of death of patients with diabetes mellitus (DM) and the sign of its decompensation. The main mechanisms that form a ground of pathogenesis of diabetic nephropathy are – creation of the products of incomplete glycosylation, disorders in the system of vitamin D3.
Aim: to study the links and levels of metabolic disorders in children with DM type 1 and at diabetic nephropathy.
Material and methods: 26 children I0–16 years old with DM type 1 and diabetic nephropathy were examined during the study. An affinity of hemoglobin to oxygen and oxidation of lipids was defined using the method of spectrophotometry. The levels of cellular hypoxia marker HIF-1 was defined with Western Blotting method.
Results: In the group of children with firstly detected DM type 1 the high level of dissociation of hemoglobin and oxygen comparing with the control group was detected. In the group of children with developed diabetic nephropathy the level of marker was considerably lower than in the control group and patients with DM type 1. The high level of intracellular hypoxia was fixed in all patients comparing with the control. HIF-1 level was considerably higher in patients with nephropathy than in the group with DM type 1. 1 It was detected an increase of lipids oxidation coefficient depending on the level of compensation of DM type 1.
Discussion: We have studied the node indicators of base metabolic and hypoxic disorders in patients with DM type 1 and patients with diabetic nephropathy. The further study of markers and its interdependence in the network of disorders caused by the deficiency of vitamin D3 and disorders in system of apoptosis control especially in aspect of diabetic nephropathy progressing is a promising direction of prophylaxis schemes creation and diabetic nephropathy treatment
References
Rojas, A., Morales, M. A. (2004). Advanced glycation and endothelial functions: A link towards vascular complications in diabetes. Life Sciences, 76 (7), 715–730. doi: 10.1016/j.lfs.2004.09.011
American Diabetes Association Standarts Of Medical Care In Diabetes (2015). The journal of clinical and applied research and education, 38, 1. Available at: http://diabetes.teithe.gr/UsersFiles/entypa/STANDARDS%20OF%20MEDICAL%20CARE%20IN%20DIABETES%202015.pdf
Vinod, P. B. (2012). Pathophysiology of diabetic nephropathy. Clinical Queries: Nephrology, 1 (2), 121–126. doi: 10.1016/S2211-9477(12)70005-5
Heilig, C. W., Deb, D. K., Abdul, A., Riaz, H., James, L. R., Salameh, J., Nahman, N. S. (2013). GLUT1 Regulation of the Pro-Sclerotic Mediators of Diabetic Nephropathy. American Journal of Nephrology, 38 (1), 39–49. doi: 10.1159/000351989
Ziyadeh, F. N., Hoffman, B. B., Han, D. C., Iglesias-de la Cruz, M. C., Hong, S. W., Isono, M. et. al. (2000). Long-term prevention of renal insufficiency, excess matrix gene expression, and glomerular mesangial matrix expansion by treatment with monoclonal antitransforming growth factor-beta antibody in db/db diabetic mice. Proceedings of the National Academy of Sciences, 97 (14), 8015–8020. doi: 10.1073/pnas.120055097
Wolf, G. Wolf, G., Ziyadeh, F. N. (2007). Cellular and Molecular Mechanisms of Proteinuria in Diabetic Nephropathy. Nephron Physiology, 106 (2), p26–p31. doi: 10.1159/000101797
Hadjadj, S., Tarnow, L., Forsblom, C., Kazeem, G., Marre, M., Groop et. al (2007). Association between Angiotensin-Converting Enzyme Gene Polymorphisms and Diabetic Nephropathy: Case-Control, Haplotype, and Family-Based Study in Three European Populations. Journal of the American Society of Nephrology, 18 (4), 1284–1291. doi: 10.1681/ASN.2006101102
Atkins, R. C., Zimmet, P. (2010). Diabetic kidney disease: act now or pay later. Journal of the American Society of Hypertension, 4 (1), 3–6. doi: 10.1016/j.jash.2009.12.001
Forbes, J. M. (2003). The breakdown of pre-existing advanced glycation end products is associated with reduced renal fibrosis in experimental diabetes. The FASEB Journal, 29 (6). doi: 10.1096/fj.02-1102fje
Chowdhury, R., Kunutsor, S., Vitezova, A., Oliver-Williams, C., Chowdhury, S., Kiefte-de-Jong, J. C. et. al (2014). Vitamin D and risk of cause specific death: systematic review and meta-analysis of observational cohort and randomised intervention studies. British Medical Journal, 348 (apr01 2), g1903–g1903. doi: 10.1136/bmj.g1903
Ivanov, Yu. G. (1975). Modifikatsiya spektrofotometricheskogo metoda opredeleniya kislorodnodissotsiatsionnykh krivykh gemoglobina. Byul. eksperimental'noy biologii i meditsiny, 79 (11), 122–123.
Pacher, P., Beckman, J. S., Liaudet, L. (2007). Nitric Oxide and Peroxynitrite in Health and Disease. Physiological Reviews, 87 (1), 315–424. doi: 10.1152/physrev.00029.2006
Hayashi, A., Suzuki, T., Shin, M. (1973). An enzymic reduction system for metmyoglobin and methemoglobin, and its application to functional studies of oxygen carriers. Biochimica et Biophysica Acta (BBA) – Protein Structure, 310 (2), 309–316. doi: 10.1016/0005-2795(73)90110-4
Shapiro, R., McManus, M. J., Zalut, C., Bunn, H. F. (1980). Sites of non-enzymatic glycosylation of human haemoglobin. J. Brit. Chem., 255 (7), 3120–3127.
Inoguchi, T., Li, P., Umeda, F., Yu, H. Y., Kakimoto, M., Imamura, M. et. al (2000). High glucose level and free fatty acid stimulate reactive oxygen species production through protein kinase C--dependent activation of NAD(P)H oxidase in cultured vascular cells. Diabetes, 49 (11), 1939–1945. doi: 10.2337/diabetes.49.11.1939
Artyukhov, V. G. (1995). Gemoproteidy: zakonomernosti fotokhimicheskikh prevrashcheniy v usloviyakh razlichnogo mikrookruzheniya. Voronezh: Izdatelstvo Voronezhskogo universitetata, 280.
Alinejad-Mofrad, S., Foadoddini, M., Saadatjoo, S. A., Shayesteh, M. (2015). Improvement of glucose and lipid profile status with Aloe vera in pre-diabetic subjects: a randomized controlled-trial. Journal of Diabetes & Metabolic Disorders, 14 (1), 2–7. doi: 10.1186/s40200-015-0137-2
Reidy, K., Kang, H. M., Hostetter, T., Susztak, K. (2014). Molecular mechanisms of diabetic kidney disease. Journal of Clinical Investigation, 124 (6), 2333–2340. doi: 10.1172/jci72271
Holick, M. F. (2007). Medical progress: Vitamin D deficiency. The New England Journal of Medicine, 357 (3), 266–281. doi: 10.1056/nejmra070553
Goldin, A., Beckman, J. A., Schmidt, A. M., Creager, M. A. (2006). Advanced Glycation End Products: Sparking the Development of Diabetic Vascular Injury. Circulation, 114 (6), 597–605. doi: 10.1161/circulationaha.106.621854
Oh, J., Weng, S., Felton, S. K., Bhandare, S., Riek, A., Butler, B. et. al. (2009). 1,25(OH)2 Vitamin D Inhibits Foam Cell Formation and Suppresses Macrophage Cholesterol Uptake in Patients With Type 2 Diabetes Mellitus. Circulation, 120 (8), 687–698. doi: 10.1161/circulationaha.109.856070
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