The Effect of Gliflozin Therapy on TNF-α Secretion by Cultured Monocytes in Patients with Diabetes

Currently it’s well established that chronic inflammation is a key pathogenetic mechanism in the development of Type 2 diabetes. The study aims to explore the inflammatory response of monocytes in diabetic patients compared to healthy subjects, focusing on TNF-α and to investigate the impact of SGLT2 inhibitors on monocyte inflammation. The study included 20 patients with newly diagnosed type 2 diabetes and 20 control subjects aged 50-79 years old, all participants provided written informed consent upon the inclusion. The secretion of pro-inflammatory cytokine TNF-α in both non-stimulated and LPS-stimulated conditions by blood-derived monocytes at baseline and after 3 months of dapagliflozin therapy 10 mg daily was assessed. Monocytes were isolated using Ficoll gradient centrifugation and CD14+ cell magnetic separation. TNF-α concentration was measured using ELISA. Diabetic patients showed a significant increase in TNF-α secretion by cultured monocytes (both non-stimulated and LPS-stimulated) compared to control subjects. After a 3-month dapagliflozin therapy, there was a significant reduction in TNF-α secretion. The study concludes that monocytes in diabetic individuals exhibit pro-inflammatory activation. Additionally, the antidiabetic therapy using SGLT2 inhibitors showed efficacy in reducing the pro-inflammatory status of monocytes. This suggests that SGLT2 inhibitors could be beneficial not only for controlling glucose levels but also for preventing diabetes-associated diseases by addressing inflammation.