Association between elevated serum uric acid levels and islet beta cell function indices in newly diagnosed type 2 diabetes mellitus-a one year cross sectional study at tertiary care center
DOI:
https://doi.org/10.18203/2320-6012.ijrms20231784Keywords:
Newly diagnosed T2DM, SUA, Pancreatic islet β cell function, HOMA-IRAbstract
Background: Serum uric acid (SUA) has been reported as a risk factor for type 2 diabetes mellitus (T2DM). Even though various studies concluded that SUA plays an essential role in DM onset, association between SUA and pancreatic islet β cell function and the effect of gender and body mass index (BMI) on it in is still unclear.
Methods: A hospital based one-year cross-sectional study was conducted and required data was collected from 76 patient who were newly diagnosed T2DM. All patients were investigated for SUA, and homeostasis model assessment-insulin resistance (HOMA-IR) was calculated using the HOMA2 calculator.
Results: Mean SUA level among the males was 4.65±1.81 mg/dl and among the females was 4.31±1.94 mg/dl. β pancreatic cell function index was estimated using HOMA-IR. Mean HOMA-IR level among the male study population was 5.01±7.44 and 5.02±4.63 among the females. A positive and significant correlation was observed between SUA and HOMA-IR (r=0.2283, p=0.0489) at 5% level, and was more pronounced among the female population (r=0.5127, p=0.0175). Correlation between HOMA-IR and BMI was found to be positive and significant (r=0.4948, p=0.0001). On plotting multiple regression analysis, coefficient of determination (R²) was 0.8374 (p<0.05), indicating significant contribution of all variables when combined towards HOMA-IR.
Conclusions: Present study demonstrates that SUA harbours a positive and significant correlation with pancreatic islet β cell function index among newly diagnosed T2DM patients and is influenced by gender and BMI.
Metrics
References
Cho NH, Shaw JE, Karuranga S, Huang Y, da Rocha Fernandes JD, Ohlrogge AW, et al. IDF Diabetes Atlas: Global estimates of diabetes prevalence for 2017 and projections for 2045. Diabetes Res Clin Practice. 2018;138:271-81.
Van Dieren S, Beulens JWJ, Kengne AP, Peelen LM, Rutten GEHM, Woodward M, et al. Prediction models for the risk of cardiovascular disease in patients with type 2 diabetes: a systematic review. Heart. 2012;98(5):360-9.
Deshpande AD, Harris-Hayes M, Schootman M. Epidemiology of diabetes and diabetes-related complications. Physical Therapy. 2008;88(11):1254-64.
Weyer C, Bogardus C, Mott DM, Pratley RE. The natural history of insulin secretory dysfunction and insulin resistance in the pathogenesis of type 2 diabetes mellitus. J Clin Invest. 1999;104(6):787-94.
Weir GC, Bonner-Weir S. Five stages of evolving beta-cell dysfunction during progression to diabetes. Diabetes. 2004;53(3):S16-21.
Lytvyn Y, Perkins BA, Cherney DZI. Uric acid as a biomarker and a therapeutic target in diabetes. Canadian J Diabetes. 2015;39(3):239-46.
Alvarez-Lario B, Macarron-Vicente J. Uric acid and evolution. Rheumatology. 2010;49(11):2010-5.
Giri AK, Banerjee P, Chakraborty S, Kauser Y, Undru A, Roy S, et al. Genome wide association study of uric acid in Indian population and interaction of identified variants with Type 2 diabetes. Sci Rep. 2016;6(1):21440.
Ishizaka N, Ishizaka Y, Toda E-I, Nagai R, Yamakado M. Association between serum uric acid, metabolic syndrome, and carotid atherosclerosis in Japanese individuals. ATVB. 2005;25(5):1038-44.
Ford ES, Li C, Cook S, Choi HK. Serum concentrations of uric acid and the metabolic syndrome among us children and adolescents. Circulation. 2007;115(19):2526-32.
Johnson RJ, Merriman T, Lanaspa MA. Causal or noncausal relationship of uric acid with diabetes. Diabetes. 2015;64(8):2720-2.
Dehghan A, van Hoek M, Sijbrands EJG, Hofman A, Witteman JCM. High serum uric acid as a novel risk factor for type 2 diabetes. Diabetes Care. 2008;31(2):361-2.
Zhang Y, Yamamoto T, Hisatome I, Li Y, Cheng W, Sun N, et al. Uric acid induces oxidative stress and growth inhibition by activating adenosine monophosphate-activated protein kinase and extracellular signal-regulated kinase signal pathways in pancreatic β cells. Mol Cell Endocrinol. 2013;375(1-2):89-96.
Ozougwu O. The pathogenesis and pathophysiology of type 1 and type 2 diabetes mellitus. J Physiol Pathophysiol. 2013;4(4):46-57.
Jia L, Xing J, Ding Y, Shen Y, Shi X, Ren W, et al. Hyperuricemia causes pancreatic β-cell death and dysfunction through nf-κb signaling pathway. Song L, editor. PLoS One. 2013;8(10):e78284.
Kivity S, Kopel E, Steinlauf S, Segev S, Sidi Y, Olchovsky D. The association between serum uric acid and diabetes mellitus is stronger in women. J Women’s Health. 2013;22(9):782-9.
Hu Y, Liu J, Li H, Zhu H, Liu L, Yuan Y, et al. The association between elevated serum uric acid levels and islet β-cell function indexes in newly diagnosed type 2 diabetes mellitus: a cross-sectional study. Peer J. 2018;6:e4515.
Tang W, Fu Q, Zhang Q, Sun M, Gao Y, Liu X, et al. The association between serum uric acid and residual β -cell function in type 2 diabetes. J Diabetes Res. 2014;2014:1-9.
Juraschek SP, McAdams-Demarco M, Miller ER, Gelber AC, Maynard JW, Pankow JS, et al. Temporal relationship between uric acid concentration and risk of diabetes in a community-based study population. Am J Epidemiol. 2014;179(6):684-91.