Research Article Sodium-Glucose Cotransporter-2 (SGLT-2) Attenuates Serum Uric Acid (SUA) Level in Patients with Type 2 Diabetes Mazhar Hussain , 1 Asim Elahi, 2 Abid Hussain, 3 Javed Iqbal, 4 Lubna Akhtar, 1 and Abdul Majid 5 1 Department of Pharmacology & Therapeutics Sheikh Zayed Medical College/Hospital, Rahim Yar Khan, Punjab, Pakistan 2 Department of Medicine CHI Saint Joseph Health Hospital, London, Kentucky, USA 3 Department of Nephrology Sheikh Zayed Medical College/Hospital, Rahim Yar Khan, Pakistan 4 Department of Medicine Sheikh Zayed Medical College/Hospital, Rahim Yar Khan, Pakistan 5 Department of Cardiology, Sheikh Zayed Medical College & Hospital Rahim Yar Khan, Pakistan Correspondence should be addressed to Mazhar Hussain; mazharhussain214@gmail.com Received 4 April 2021; Revised 15 May 2021; Accepted 8 June 2021; Published 19 June 2021 Academic Editor: Claudia Cardoso Copyright © 2021 Mazhar Hussain et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Background. Hyperuricemia has a strong association with diabetes mellitus. Hyperuricemia can lead to cardiovascular and renal complications in patients with diabetes. The goal of this study was to compare the effect of sodium-glucose cotransporter-2 (SGLT-2) inhibitors dapagliflozin and empagliflozin on serum uric acid (SUA) levels in patients with type 2 diabetes against traditional oral antihyperglycemic drugs (OADs). Methods. In this double-blind randomized controlled trial, 70 patients with type 2 diabetes and elevated SUA levels were assigned to two treatment groups. Patients in group A received SGLT-2 inhibitors tablet dapagliflozin 5 mg to 10 mg and empagliflozin 10 mg to 25 mg. Group B patients received OADs such as glimepiride, metformin, sitagliptin, gliclazide, and glibenclamide as monotherapy or combination therapy. The changes in SUA level were primary end points while changes in body weight and body mass index (BMI) from baseline to end point were secondary end points. Results. After four weeks of treatment, we noted a significant reduction of mean SUA levels in the SGLT-2 inhibitor group from 7:5±2:5 to 6:3±0:8 mg/dl versus comparator group from 7:1±1:8 to 6:8±2:2 mg/dl (p =0:001). Mean body weight was significantly reduced in the SGLT-2 group from 82 ± 10:4 to 78 ± 12:5 kg versus comparator group from 78 ± 13:2 to 79:2±9:7 kg (p =0:001). Similarly, the mean BMI of patients in the SGLT-2 group was significantly reduced from 25:7±3:2 to 24:2±3:2 kg/m 2 versus comparator group from 27:5±4:2 to 28 ± 3:6 kg/m 2 (p =0:002). Conclusion. SGLT-2 inhibitors have a strong potential to decrease SUA levels in patients with type 2 diabetes. 1. Introduction The prevalence of diabetes is growing worldwide and con- tinues to represent a global health challenge. In 2015, the esti- mated prevalence of diabetes was 8.8%, but projections estimate this will rise to 10.4% by 2040 [1].The International Diabetes Federation estimates that the number of patients with diabetes will reach 552 million in 2030, adding signifi- cant morbidity and mortality for patients and social and economic burdens on health systems. Identifying and pre- venting risk factors for diabetes are urgent to stop the diabe- tes epidemic [2]. Hyperuricemia is a disorder of purine metabolism. Serum uric acid (SUA) levels are usually elevated in patients with diabetes compared to healthy individuals. Hyperurice- mia increases the risk of diabetes in people who have impaired glucose tolerance, and hyperuricemia is highly prevalent in patients with diabetes [3, 4]. SUA is a strong independent, novel risk factor for diabetes [5]. Increases in body weight, waist circumference, dyslipidemia, sedentary lifestyle, hypertension, and insulin resistance are predispos- ing factors for hyperuricemia in patients with diabetes [6, 7]. Hyperuricemia has a strong association with type 2 dia- betes and is a strong predictor for developing metabolic Hindawi Journal of Diabetes Research Volume 2021, Article ID 9973862, 5 pages https://doi.org/10.1155/2021/9973862