Abstract
Background: several randomized clinical trials have demonstrated that dapagliflozin, like other inhibitors of sodium-glucose cotransporter 2 (SGLT2), significantly improves cardiovascular and renal outcomes in type 2 diabetes (T2D). However, underlying mechanisms remain unclear. Aim: to assess changes in the levels of serum markers associated with fibrosis and inflammation in patients with T2D receiving dapagliflozin. Patients and Methods: this prospective single-center study included 27 patients aged 40–65 years with T2D that lasts more than 1 year and without verified atherosclerosis but multiple cardiovascular risk factors (i.e., dyslipidemia, obesity, hypertension). In addition to basic treatment for T2D, all patients received dapagliflozin 10 mg daily for 6 months. Before and 6 months after treatment, the levels of the markers of fibrosis (including procollagen type I carboxy-terminal propeptide/PICP) and inflammation were measured. Results: the median age was 56 [49; 61] years and the median duration of T2D was 7 [4; 12] years. After 6-month treatment with dapagliflozin, significant reduction in the concentration of PICP from 136.8 [100,4; 200,6] ng/ml to 104.8 [79.7; 162.0] ng/ml (р = 0.019). The levels of galectin-3, matrix metalloproteinase (MMP) 9, tissue inhibitor of MMP-1, growth stimulating expressed gene 2, high-sensitivity C-reactive protein, and N-terminal pro-atrial natriuretic peptide were similar at baseline and after 6-month treatment. Conclusions: 6-month treatment with dapagliflozin reduced the levels of PICP. Together with other mechanisms, this phenomenon illustrates the positive effects of dapagliflozin on cardiovascular and renal outcomes in T2D. KEYWORDS: type 2 diabetes, fibrosis, chronic inflammation, dapagliflozin, cardiovascular diseases. FOR CITATION: Lebedev D.A., Babenko A.Yu. Effects of dapagliflozin of the markers of fibrosis and inflammation in type 2 diabetes and very high cardiovascular risk. Russian Medical Inquiry. 2021;5(4):185–188 (in Russ.). DOI: 10.32364/2587-6821-2021-5-4-185-188.
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