Abstract
Glucose is a main energy source for ATP production and its effective utilization is important to maintain homeostasis. Although glucose is filtrated in glomerulus, sodium glucose co–transporter 1/2 (SGLT1/2) in the renal tubules reabsorbs it. SGLT2 selectively expresses in the proximal tubules and reabsorbs a large fraction of glucose, while SGLT1 exists in the kidney and small intestine to take up both glucose and galactose. Accordingly, SGLT2 inhibition could block glucose reabsorption and, indeed, SGLT2 inhibitors show the expected effects. Importantly, human SGLT2 deficiency or SGLT2 knockout mice show no remarkable phenotypes except renal glycosuria, supporting that SGLT2 inhibitors could be relatively safe. In addition, recent studies reveal that treatment with SGLT2 inhibitors improves a variety of metabolic syndromes, such as nonalcoholic steatosis, atherosclerosis and diabetic nephropathy.
In this review, we introduce the characterization of SGLT2 and the effect of SGLT2 inhibitors on metabolic syndromes.
