Effect of Uric Acid on Blood Glucose Levels
Keywords:
high uric acid level, nitric oxide, oxidative stress, blood glucoseAbstract
Uric acid as the final result of purine bases metabolism. In high level condition, uric acid enters the cell and act as oxidant, and acts as independent risk factor and predicts the incident of type 2 diabetes mellitus (T2DM). It may directly inactivate or through oxidative reaction that lower the nitric oxide (NO) level. Lower NO level will reduce insulin uptake in tissues and reduce in GLUT4 translocation in cell that will effect the blood glucose level. The High level of uric acid or hyperuricemia makes oxidative stress by inducing the production of reactive oxygen species (ROS) which interferes the insulin signalling pathway,creates inflammatory state that reduced the insulin sensitivity,blood glucose uptake and metabolism, also reducing the insulin production from pancreatic islet cells.References
Davison A, Milan A, Philips S, Ranganath L. Nucleic acids. Biochemistry and metabolism. London: JP Medical Ltd; 2015. p. 43-68.
Jin M, Yang Fan, Yang I, et al. Uric acid, hyperuricemia and vascular diseases. Front Biosci (Landmark Ed). 2012;17:656-69.
Basaran N,Evliyaoglu O, Sucu V, et al. Changing of uric acid levels by age and sex in patients with diabetes mellitus. J Clin Exp Invest. 2016;7(1):1-6.
Johnson RJ, Nakagawa T, Gabriela Sanchez-Lozada L, et al. Sugar, uric acid, and etiology of diabetes and obesity. Diabetes. 2013;62:3307-15.
Ray D, Kundu D, Choudhury DG, et al. Relation of elevated serum adenosine deaminase levels to glycated hemoglobin and serum uric acid in type 2 diabetes mellitus. Int J Med Res Review. 2016;4(7):1148-54.
Miyaje T, Kumagi T, Furukawa S, et al. Hyperuricemia is a risk factor for the onset of impaired fasting glucose in men with a high plasma glucose level: a community-based study. Plos ONE. 2014;9(9):e107882.
Wang H, Wang AX, Aylor K, Barrett EJ. Nitric oxide directly promotes vascilar endothelial insulin transport. Diabetes. 2013;62:4030-42.
Merry TL, McConell GK. Skeletal muscle glucose uptake during exercise: a focus on reactive oxygen species and nitric oxide signaling. IUBMB Life. 2009;61(5):479-84.
Acharya CR, Sharma AK, Kantaria ND. Involvement of oxidative stress in patients of gout and antioxidant effect of allopurinol. Int J Med Sci Public Health. 2015;4(2):168-72.
Magenta A, Greco S, Capogrossi M, et al. Nitric oxide, oxidative stress, and p66shc interplay in diabetic endothelial dysfunction. Biomed Res Int. 2014;Article ID 193095:16.
Ozcan A,Ogun M. Biochemistry of reactive oxygen and nitrogen species. In: Gowder SJT, ed. Basic principles and clinical significance of oxidative stress. InTech; 2015. DOI: 10.5772/61193.
Zhi L, Yuzhang Z, Tianliang H, et al. High uric acid induces insulin resistance in cardiomyocytes in vitro and in vivo. Plos ONE. 2016;11(2):e0147737.
Droge W. Free radicals in the physiological control of cell function. Physiol Rev. 2002;82:47-95.
Bender SB, McGraw AP, Jaffe IZ, Sowers JR. Mineralocorticoid receptor-mediated vascular insulin resistance. An early contributor to diabetes-related vascular disease? Diabetes. 2013;63:313-9.
Baldwin W, McRae S, Marek G, et al. Hyperuricemia as a mediator of the proinflammatory endocrine imbalance in the adipose tissue in a murine model of the metabolic syndrome. Diabetes. 2011;60:1258-69.
Du Toit EF, Donner DG. Myocardial insulin resistance: an overview of its causes, effects, and potential therapy, insulin resistance. In: Dr. Sarika Arora, ed. Insulin resistance. InTech; 2012. DOI: 10.5772/50619.
Cai W, Mei Duan X, Liu Y, et al. Uric acid induces endothelial dysfunction by activating by HMGB1/RAGE signaling pathway. BioMed Res Int. 2016;2017:Article ID 4391920.
Matsouka T, Kaneto H, Miyatsuka T, et al. Regulation of mafA expression in pancreatic ?-cells in db/db mice with diabetes. Diabetes. 2010;59:1709-20.
Jia L, Xing J, Ding Y, et al. Hyperuricemia causes pancreatic ?-cell death and dysfunction through NF-?? signaling pathway. Plos ONE. 2013;8(10):e78284.
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