A systematic review examining the effects of sodium-glucose cotransporter-2 inhibitors (SGLT2is) on biomarkers of inflammation and oxidative stress. (October 2020)

• Record Type: Journal Article
• Authors: Bray, Jonathan J.H.; Foster-Davies, Harri; Stephens, Jeffrey W.
• Is Part Of: Diabetes research and clinical practice. Volume 168(2020)
• Publication Date: 2020-10
• Subjects: Inflammation -- Oxidative stress, type 2 diabetes -- Sodium-glucose cotransporter-2 inhibitors; Diabetes -- Periodicals; Diabetes Mellitus -- Periodicals; 616.462
• DOI: 10.1016/j.diabres.2020.108368
• Languages: English
• ISSNs: 0168-8227

Abstract

Abstract: Aims: Sodium-glucose cotransporter-2 inhibitors (SGLT2is) have a protective cardiorenal effect in type 2 diabetes. This systematic review examines the effects of SGLT2is on clinical biomarkers of inflammation and oxidative stress. Methods: A search of Medline, Embase, Web of Science, and The Cochrane Library was performed examining changes in selected clinical biomarkers for inflammation: c-reactive protein (CRP), adiponectin, interleukin-6 (IL6), tumour necrosis factor-alpha (TNF-α), and oxidative stress: 8- iso -prostaglandin F2α (8- iso -PGF2α) and 8-hydroxy-2′-deoxyguanosine (8-OHdG). Quality of evidence was evaluated using the GRADEpro tool and risk of bias was assessed using the Cochrane RoB 2 and ROBINS-I tools. Results: A total of 23 (15 randomised, 8 observational) heterogeneously-designed clinical studies were identified (1654 patients, 24 weeks median follow-up). Consistent reductions were observed for CRP (10/12 studies), IL6 (5/5 studies), TNFα (3/4 studies), 8- iso -PGF2α (3/4 studies) and 8-OHdG (2/2 studies), and a consistent increase in adiponectin (6/8 studies). Change in serum CRP following SGLT2is appear to be independent of change in HbA1c and other study design and clinically relevant variables. Conclusions: There is heterogeneous, yet consistent data supporting the beneficial effects of SLGT2is on inflammatory and oxidative stress. Change in serum CRP appears to be independent of change in HbA1c.