Renal glucose reabsorption inhibitors to treat diabetes

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Current therapies to reduce hyperglycaemia in type 2 diabetes mellitus (T2DM) mostly involve insulin-dependent mechanisms and lose their effectiveness as pancreatic ß-cell function declines. In the kidney, filtered glucose is reabsorbed mainly via the high-capacity, low-affinity sodium glucose cotransporter-2 (SGLT2) at the luminal surface of cells lining the first segment of the proximal tubules. Selective inhibitors of SGLT2 reduce glucose reabsorption, causing excess glucose to be eliminated in the urine; this decreases plasma glucose. In T2DM, the glucosuria produced by SGLT2 inhibitors is associated with weight loss, and mild osmotic diuresis might assist a reduction in blood pressure. The mechanism is independent of insulin and carries a low risk of hypoglycaemia. This review examines the potential of SGLT2 inhibitors as a novel approach to the treatment of hyperglycaemia in T2DM.
Original languageEnglish
Pages (from-to)63-71
Number of pages9
JournalTrends in Pharmacological Sciences
Issue number2
Early online date4 Jan 2011
Publication statusPublished - Feb 2011


  • animals
  • type 2 diabetes mellitus
  • glucose
  • humans
  • hypoglycemic agents
  • kidney
  • membrane transport modulators
  • sodium-glucose transporter 2


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