Abstract
Physiologically, urine from the subject with normal kidney function does not contain detectable level of glucose unless otherwise renal glycosuria. Sodium glucose transporter (SGLT) families in proximal tubules of the kidney play detrimental role to reabsorb the filtered glucose. Recently, the inhibitors for the SGLT2 are available for clinical use for purposing the urinary glucose excretion and lowering blood glucose level. Unexpectedly, the SGLT2 inhibitors have become famous for its cardio-renal protective effects with unknown mechanism. We have so far explored how its inhibition changes cell fate, how the drug affects glucose uptake in non-diabetic kidney, and if the drug suppresses the development of fibrosis. In this review, we will summarize our findings and provide the remaining questions.
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