Fig. 1.

Mechanism of action of SGLT2is. The basic mechanism of action of SGLT2is is to inhibit the active transport of glucose by SGLT2 in the luminal surface of the S1 segment of the proximal renal tubule which is linked to Na⁺ transport maintained by its active extrusion. The latter process takes place with the participation of Na⁺/ATPase of the cell membrane. Under normal circumstances, in the glomeruli of the kidneys, large quantities, about 180 g/day, of glucose are constantly filtering into the primary urine. Then, it is reabsorbed in the proximal tubule with the participation of SGLT2 (90%) and to a lesser extent with the participation of SGLT1 (10%). SGLT2is significantly reduce glucose reabsorption from primary urine at the level of the proximal tubule and thus induce glucosuria, lowering plasma glucose concentration in a mechanism independent of insulin. Simultaneously with glucosuria, SGLT2 inhibitors intensify the excretion of sodium, which is cotransported with glucose and which, in turn, causes an increase in osmotic diuresis. This unique mechanism of SGLT2is action results in numerous non-glycaemic effects throughout the body. SGLT1 sodium-glucose cotransporter-1, SGLT2 sodium-glucose cotransporter-2, SGLT2is sodium-glucose cotransporter-2 inhibitors