SGLT2i: beyond the glucose-lowering effect- A review
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Type 2 diabetes (T2DM) is a metabolic disease that is commonly associated with obesity, dyslipidemia, hypertension, heart failure, hyperuricemia, renal failure and hyperuricemia and affects individuals worldwide. In addition, patients with T2DM have an increased risk of cardiovascular or renal complications, which are leading causes of morbidity and mortality. Although several oral and intravenous glucose-control drugs have been widely used, concerns about cardiorenal complications in these populations still attract considerable attention.

Therefore, a more comprehensive approach to cardiovascular and renal risk management in T2DM has emerged. Sodium/glucose cotransporter-2 inhibitors (SGLT2i) block SGLT2 located in the early proximal renal tubule, which leads to increased urinary glucose excretion and subsequently decreased serum glucose concentrations.

These glucose-lowering effects are independent of insulin action. To date, SGLT2i has been demonstrated to reduce major adverse cardiovascular events and hospitalization for heart failure. In addition, these drugs showed surprising effects on the progression of renal complications, such as lowering serum creatinine, reducing albuminuria, and decreasing death due to renal disease.

Interestingly, these cardiorenal protective effects appear to be independent of glucose-control efficacy. Considering these encouraging findings, SGLT2i are highly recommended for patients with T2DM with high cardiovascular or renal risks. Therefore, the mechanisms that drive the cardiorenal protection of SGLT2i should be elucidated.

This review aims to provide an update on the extraglycemic effects of SGLT2i that may contribute to cardiorenal protection.