Phloretin inhibits the active transport of glucose into cells by SGLT1 and SGLT2, though the inhibition is weaker than by its glycosidephlorizin. Orally consumed phlorizin is nearly entirely converted into phloretin by hydrolytic enzymes in the small intestine. An important effect of this is the inhibition of glucose absorption by the small intestine and the inhibition of renal glucose reabsorption. Phloretin also inhibits a variety of urea transporters. It induces urea loss and diuresis when coupled with high protein diets.
^ abIdris, I.; Donnelly, R. (2009). "Sodium-glucose co-transporter-2 inhibitors: An emerging new class of oral antidiabetic drug". Diabetes, Obesity and Metabolism11 (2): 79. doi:10.1111/j.1463-1326.2008.00982.x.edit
^ abCrespy, V.; Aprikian, O.; Morand, C.; Besson, C.; Manach, C.; Demigné, C.; Rémésy, C. (2001). "Bioavailability of phloretin and phloridzin in rats". The Journal of nutrition131 (12): 3227–3230. PMID11739871.edit