Volume 19, Issue 1 (1-2020)
ijdld 2020, 19(1): 44-50 |
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Moradi Z, Ravari M S, Farrokhi E, Hashemzadeh Chaleshtori M. INVESTIGATION OF METHYLATION OF TNF-Α GENE PROMOTER IN PATIENTS WITH TYPE 2 DIABETES. ijdld 2020; 19 (1) :44-50
URL: http://ijdld.tums.ac.ir/article-1-5866-en.html
URL: http://ijdld.tums.ac.ir/article-1-5866-en.html
1- Wu Y, Ding Y, Tanaka Y, Zhang W. Risk factors contributing to type 2 diabetes and recent advances in the treatment and prevention. Int J Med Sci 2014; 11(11):1185-200. 2. Zheng Y, Ley SH, Hu FB. Global aetiology and epidemiology of type 2 diabetes mellitus and its complications. Nature Reviews Endocrinology [Review Article]. 2017; 14:88. 3. Kameswaran V, Bramswig NC, McKenna LB, Penn M, Schug J, Hand NJ, et al. Epigenetic regulation of the DLK1-MEG3 microRNA cluster in human type 2 diabetic islets. Cell Metab 2014; 19(1):135-45. 4. Kwak SH, Park KS. Recent progress in genetic and epigenetic research on type 2 diabetes. Exp Mol Med 2016; 48:e220. 5. Nilsson E, Ling C. DNA methylation links genetics, fetal environment, and an unhealthy lifestyle to the development of type 2 diabetes. Clin Epigenetics 2017; 9:105. 6. Makki K, Froguel P, Wolowczuk I. Adipose tissue in obesity-related inflammation and insulin resistance: cells, cytokines, and chemokines. ISRN Inflamm 2013; 2013:139239 7. Kahn SE, Hull RL, Utzschneider KM. Mechanisms linking obesity to insulin resistance and type 2 diabetes. Nature 2006; 444(7121):840-6. 8. Nicholas DA, Andrieu G, Strissel KJ, Nikolajczyk BS, Denis GV. BET bromodomain proteins and epigenetic regulation of inflammation: implications for type 2 diabetes and breast cancer. Cell Mol Life Sci 2017; 74(2):231-43. 9. Sommese L, Zullo A, Mancini FP, Fabbricini R, Soricelli A, Napoli C. Clinical relevance of epigenetics in the onset and management of type 2 diabetes mellitus. Epigenetics 2017; 12(6):401-15. 10. Al Muftah WA, Al-Shafai M, Zaghlool SB, Visconti A, Tsai P-C, Kumar P, et al. Epigenetic associations of type 2 diabetes and BMI in an Arab population. Clinical epigenetics 2016; 8: 13. 11. Akash MSH, Rehman K, Liaqat A. Tumor Necrosis Factor-Alpha: Role in Development of Insulin Resistance and Pathogenesis of Type 2 Diabetes Mellitus. J Cell Biochem 2018; 119(1):105-10. 12. Miao F, Gonzalo IG, Lanting L, Natarajan R. In vivo chromatin remodeling events leading to inflammatory gene transcription under diabetic conditions. J Biol Chem 2004; 279(17):18091-7. 13. Hermsdorff HH, Mansego ML, Campión J, Milagro FI, Zulet MA, Martínez JA. TNF-alpha promoter methylation in peripheral white blood cells: Relationship with circulating TNFα, truncal fat and n-6 PUFA intake in young women. Cytokine 2013; 64(1):265-71. 14. Liu C, Feng X, Li Q, Wang Y, Li Q, Hua M. Adiponectin, TNF-alpha and inflammatory cytokines and risk of type 2 diabetes: A systematic review and meta-analysis. Cytokine 2016; 86:100-9. 15. Pinzon-Cortes JA, Perna-Chaux A, Rojas-Villamizar NS, Diaz-Basabe A, Polania-Villanueva DC, Jacome MF, et al. Effect of diabetes status and hyperglycemia on global DNA methylation and hydroxymethylation. Endocr Connect 2017; 6(8):708-25
2- Department of Molecular Medicine, School of Advanced Technologies, Shahrekord University of Medical Sciences, Shahrekord, Iran ,e_farrokhi_k@yahoo.com
3- Modeling in Health Center, Shahrekord University of Medical Sciences, Shahrekord, Iran
2- Department of Molecular Medicine, School of Advanced Technologies, Shahrekord University of Medical Sciences, Shahrekord, Iran ,
3- Modeling in Health Center, Shahrekord University of Medical Sciences, Shahrekord, Iran
Abstract: (2462 Views)
Background: Type II diabetes is a chronic inflammatory condition that is associated with a combination of genetic and environmental factors. Tumor necrosis factor alpha or TNF-α as an adipocyte cytokine, which affects the signaling pathway of insulin, can contribute to insulin resistance in type 2 diabetes patients. Considering the importance of epigenetic changes in multifactorial diseases, this study aimed to investigate TNF-α promoter methylation in patients with type 2 diabetes.
Methods: This study was performed on 61 patients with type 2 diabetes and 31 non-diabetic patients. The Groups were matched in terms of demographic characteristics. The lipid profiles were measured by standard kits. TNF-α promoter methylation levels were measured by bisulphite treatment method, Nested PCR and sequencing.
Results: There was no association between TNF-α promoter methylation gene promoter and type 2 diabetes in the studied groups. Also, there was no association between TNF-α promoter methylation in diabetic and non-diabetic groups between males and females.
Conclusion: The epigenetic changes in cytokines that contribute to insulin resistance in type 2 diabetic patients seem to be ineffective in peripheral blood samples, and other tissues may need to be investigated in this regard.
Methods: This study was performed on 61 patients with type 2 diabetes and 31 non-diabetic patients. The Groups were matched in terms of demographic characteristics. The lipid profiles were measured by standard kits. TNF-α promoter methylation levels were measured by bisulphite treatment method, Nested PCR and sequencing.
Results: There was no association between TNF-α promoter methylation gene promoter and type 2 diabetes in the studied groups. Also, there was no association between TNF-α promoter methylation in diabetic and non-diabetic groups between males and females.
Conclusion: The epigenetic changes in cytokines that contribute to insulin resistance in type 2 diabetic patients seem to be ineffective in peripheral blood samples, and other tissues may need to be investigated in this regard.
Type of Study: Research |
Subject:
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Received: 2019/06/23 | Accepted: 2020/01/21 | Published: 2019/11/1
Received: 2019/06/23 | Accepted: 2020/01/21 | Published: 2019/11/1
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